GARABED EKNOYAN

THIS BOOK HAS BEEN DONATED

By Canadian Organization For Development Through

Education [CODE] And

Rotary Club of Bowmanvilla

Under Rotary World Community Service Programme

Medical Procedures Manual

GARABED EKNOYAN, M.D. Professor of Medicine

Baylor College of Medicine Houston, Texas

Illustrations by BARRY BAKER

mH P f

YEAR BOOK MEDICAL PUBLISHERS, INC. CHICAGO • LONDON

Contents

Preface ix

Acknowledgments xi

1 Lumbar Puncture 1

2 Thoracentesis 19

3 Pleural Biopsy 33

4 Abdominal Paracentesis 42

5 Peritoneal Biopsy 60

6 Bone Marrow Aspiration and Biopsy 65

7 Arthrocentesis 77

8 Sigmoidoscopy 95

9 Rectal Biopsy 106

10 Percutaneous Liver Biopsy 112

11 Transtracheal Aspiration 122

12 Peritoneal Dialysis 134

13 Endotracheal Intubation 148

14 Arterial Line Placement 156

15 Central Venous Line Placement 163

16 Flow-Directed Balloon-Tipped

(Swan-Ganz) Catheterization 182

17 Pericardiocentesis 198

18 Cardioversion 208

19 Temporary Ventricular Pacing 217

Preface

THIS BOOK represents the evolutionary outgrowth of a procedures manual first developed in 1977 at Baylor College of Medicine for the teaching of medical students and house staff. The need for such a manual was felt because of the existing discrepancy in the way trainees upon assuming clinical responsibilities were learning, per-forming, and acquiring competence in the various procedures that an internist often uses to practice his "trade." This has classically been an unstructured process, revolving around the principle of "see one, do one, then teach one," with no standard required reading or adequate documentation of "who" is teaching "what." As such, a con-siderable amount of unrecorded "folklore" and unchecked informa-tion has passed from one generation to another. To bring some uni-formity to the teaching at Baylor, it was felt that the first step should be the adoption of a standard text. Existing manuals, how-ever, covered primarily technical aspects of the various procedures; placed considerable emphasis on emergency and minor surgical pro-cedures; offered limited consideration of the indications, contraindi-cations, and complications of each procedure; but, most important, provided no information on the interpretation of the results ob-tained. Considering the diagnostic reasons for which most proce-dures are performed by the internist, this latter deficiency was a particularly glaring one that needed remedying. This led to the prep-aration of an initial in-house manual in 1977, a subsequent revision in 1979, and, finally, a complete rewriting resulting in the present text in 1981.

This book, then, is meant to be a record of the facts and folklore that previously have been passed from one generation to another. In no way could it replace the traditional way of learning through ob-servation and imitation of others. The skill of performing any pro-cedure can be acquired only from repeated exposure to it. No amount of reading of any manual can correct the unavoidable early technical incompetence. The purpose of this book is to provide some technical preparedness by pointing out errors that have been committed by others in the past, in the hope that they will be reduced in the fu-ture, and to provide a reference source on how to interpret the re-sults obtained from the performance of various procedures. None of the material included is new. It is essentially a compilation of infor-mation available in a number of different specialty textbooks but not

ix

X Preface

easily accessible under one cover in the compact form presented here.

The material presented delineates the most common and impor-tant procedures performed by students and trainees upon assuming clinical responsibility on the medical wards of every teaching insti-tution. As such, it is selective in its content and any reader may find omissions and have good reasons for feeling that one or two or more procedures should have been included. No attempt has been made to be exhaustive. Most of the material covered in the first part of the book consists of the relatively simple, primarily diagnostic, occasion-ally therapeutic procedures that every trainee in internal medicine must learn. More sophisticated emergency and life-saving proce-dures, often reserved for intensive or coronary care units, are cov-ered in the latter part of the book. Not all of these latter procedures can or should be performed by any but well-trained and experienced individuals. However, even novices should be familiar with the pro-cedures required for emergency management and be knowledgeable about the techniques they are often expected to assist in and, with further experience, perform themselves.

Each procedure is covered in a chapter that consists of five sec-tions: Indications, Contraindications, Technique, Complications, and Interpretation. For each procedure all the "do's" and "dont's" are cov-ered, the reasons "why" it is performed are explained, and an inter-pretation of the results is presented. The techniques described are the ones that have been successfully used at our institution and might differ slightly from those performed elsewhere. It would be naive to consider them the only acceptable approach.

The classical medical style of documenting every statement with references is not important in such a manual and tends to be dis-tracting to the beginner. For those whose curiosity is aroused and who wish to read further, a selected list of references appears at the end of each chapter. The sequence in which the references are grouped is similar to that of the sections of each chapter: indications, contraindications, and so on. The references are annotated both to provide summaries and to permit the better selection of particular works the reader may want to explore in greater detail in a library. The reader is encouraged to peruse the annotations. They are meant to underscore the points made in the text and to provide a selected review of the literature on the subject.

In dedicating this book to students of medicine, I am using the term in its broad sense to include not only medical students but house officers and all paramedical personnel who come in contact with patients and are directly or indirectly involved in the comple-tion of a procedure. I hope that this manual will prove useful to all those involved in patient care, whatever their current categorical title might be. Finally, I will be grateful for suggestions from any user of the manual—be he student or teacher—on how its contents might be improved.

GARABED EKNOYAN

Acknowledgments

THIS BOOK could not have been written without the help of many people during its development in the Department of Medicine of Baylor College of Medicine. In naming them, I am bound to commit the usually unforgivable sin of forgetting someone. With apologies for any omissions, I would first like to acknowledge the especially significant contributions of the following individuals who during their term of service as chief residents in the Baylor affiliated hos-pitals were instrumental in preparing the material that went into the earlier versions of the manual as used at Baylor: Carrol Cagle, Dennis Hamill, Robert Pollnow, Jay Schapira, James Shelhamer, Shelly Rubenfeld, Robert Berglund, David Miller, Dan Mulkey, David Huston, Harold Bencowitz, Russell Hoverman, Mark Sheehan, Jorge Garcia, Gordon Crofoot, William Ramsey, Robert Dillman, James B. Young, William Chamberlain, Russell Henry, Steve Keuer, William Wickemeyer, and Richard Permutt. These gentlemen were assisted by a number of the Baylor faculty in preparing the initial drafts of several of the procedures. Whatever success may be achieved by this book must be attributed to their work.

I am grateful to the following individuals for their support, advice, guidance, and invaluable assistance in reading and criticizing the first in-house version of this manual: Henry D. Mcintosh, formerly Chairman, Harold Brown, Deputy Chairman, and Robert J. Luchi, Vice Chairman of the Department of Medicine at Baylor College of Medicine; and H. Irving Schweppe, Director of the St. Luke's Epis-copal Hospital Residency Program and Clinical Professor of Medi-cine, Baylor College of Medicine.

Special recognition is due Barry Baker, who prepared the illustra-tions and patiently revised the various versions and corrections they had to go through, and to Julie Kavitski, who executed the cover design. My thanks to the staff at Year Book Medical Publishers. It was a pleasure to work with them, especially the three ladies who guided the manual through its production: Nancy Chorpenning, Joy Neuman, and Dottie Mulligan. Particular thanks go to Charlia Due, who over the six long years this book went through its evolutional process, patiently and indefatigably typed, retyped, and then typed again the innumerable revisions.

xi

xii Acknowledgments

Finally, I am especially grateful to my wife Sybil and to my chil-dren, Gregory, Byron, and Donald, who unknowingly but lovingly and patiently tolerated the anxiety, sleepless nights, and long week-ends that went into the effort of preparing this book.

G.E.

1

Lumbar Puncture

I. INDICATIONS

A. Meningitis (either bacterial, mycobacterial, viral, or fungal) Lumbar puncture is essential to the diagnosis of meningitis and this is its primary indication in the practice of internal medicine. It should be performed in every patient in whom there is a strong suspicion of meningitis because of his-tory (headache, altered state of consciousness, fever) or clini-cal setting (e.g., postcraniotomy). In patients with fever and an altered mental status, a lumbar puncture should be per-formed even if another explanation for the findings is readily apparent. Do not be disturbed by the absence of nuchal rigid-ity, which will not be present in a comatose patient and may not be present early in the course of meningitis. If a signifi-cant relative contraindication to lumbar puncture exists, take what steps are necessary to diminish the chances of a signifi-cant complication (e.g., giving platelet transfusions to throm-bocytopenic patients, or getting immediate assistance from a neurosurgeon), but obtain cerebrospinal fluid (CSF) if menin-gitis is strongly suspected.

B. Follow-up to therapy of meningitis In some patients with documented meningitis one may wish to perform a lumbar puncture after several days to confirm that the proper choice of antibiotics has been made and to demonstrate the expected response to this therapy.

C. Intrathecal antibiotics or antineoplastic chemotherapeutic agents In the treatment of gram-negative or fungal menin-gitis, it is generally necessary to administer intrathecal agents unless one is prepared to instill these drugs directly into the ventricle. Intrathecal injections of antineoplastic che-motherapeutic agents are utilized in the therapy of childhood leukemia and some other neoplastic diseases.

D. Diagnosis of tertiary syphilis A patient with latent syphilis generally should have a lumbar puncture performed to rule out neurosyphilis. This procedure is optimal in patients with

1

2 Lumbar Puncture

latent syphilis if one intends to treat the patient with a peni-cillin dose satisfactory for the treatment of neurosyphilis. If a patient has signs or symptoms suggestive of neurosyphilis, then a lumbar puncture is essential for diagnosis.

E. Subarachnoid hemorrhage It may be important to document a suspected subarachnoid hemorrhage and to differentiate it from other disease processes, e.g., meningitis, since these pa-tients often have nuchal rigidity as well as a low-grade fever.

F. Other indications Lumbar puncture is performed for the ad-ministration of spinal anesthetics, for pneumoencephalogra-phy, myelography, iodinated 1-131 serum albumin scans, for diagnosing multiple sclerosis (MS) (often associated with ele-vated CSF-"y globulin levels) and other demyelineating dis-eases, for documentation of meningeal carcinomatosis, occa-sionally to aid in the diagnosis of brain tumors, and for sev-eral other reasons. In these situations, the lumbar puncture is usually performed by someone other than an internist, e.g., an anesthesiologist, radiologist, neurologist, or neurosurgeon.

II. CONTRAINDICATIONS Each of the following is a relative con-traindication. The point to remember is not that a lumbar punc-ture should never be performed under the circumstances listed below, but rather that a puncture in each of these conditions has a known risk and the test should be strictly confined to situations in which it will provide essential information, as in meningitis. With patients in whom meningitis is strongly suspected, one must obtain CSF for examination, whether this be by lumbar puncture, cisternal tap, or lumbar puncture following other di-agnostic procedures (cerebral arteriogram or computerized axial tomography) or therapeutic maneuvers (platelet transfusion).

A. Increased intracranial pressure If increased intracranial pressure is suspected on the basis of a proven mass lesion, because of clinical findings suggestive of a mass lesion (i.e., focal neurologic findings), because of evidence of a possible brain abscess, or because of papilledema, the lumbar puncture should not be performed without the assistance of a neurosur-geon or a neurologist; and even then it should be performed preferably only after cerebral arteriography.

Categorical statements that lumbar puncture should never be done in the presence of increased intracranial pressure and especially in the presence of papilledema have been made. Most of these, however, are from the older literature and must be examined in their historical context. In early use, lumbar puncture was not limited to diagnostic studies but was utilized therapeutically to reduce increased intracranial pressure. Needles of large bore (16- to 20-gauge) were then used and

Technique 3

large quantities of fluid were removed. The rule of not per-forming lumbar puncture with increased intracranial pressure is not absolute; careful puncture using small-bore needles with the gradual removal of small quantities of fluid for di-agnostic purposes can be safely performed. Caution in per-forming a tap under these conditions should not be exagger-ated into a contraindication. The choice must depend on the relative danger of the procedure and the diagnostic informa-tion to be obtained in each individual case. Puncture should be performed only when the findings will be of aid in estab-lishing the correct diagnosis.

B. Hemorrhagic diathesis Patients with clotting factor defi-ciencies, with quantitative or qualitative platelet deficiencies, or patients undergoing treatment with anticoagulants should undergo lumbar puncture only for compelling indications, with the smallest possible needle, by the most skilled physi-cian available, and only after the clotting abnormality has been reversed to whatever extent possible by therapeutic ma-neuvers such as factor replacement, platelet transfusion, or reversal of anticoagulation.

C. Local infection Osteomyelitis of lumbar spine, epidural ab-scess, etc., should be circumvented.

III. TECHNIQUE

A. Assemble proper equipment Before beginning the proce-dure, check the tray to be certain that it contains all the equipment required. This includes the following:

1. One to two spinal needles, preferably 20- and 22-gauge. 2. At least three and preferably four sterile tubes for speci-

mens. 3. A three-way stopcock. 4. A manometer. A 20- or 22-gauge needle is preferred. It has been demon-

strated that the use of a smaller needle is less likely to pro-duce a postspinal headache. The 22-gauge needle is more dif-ficult to use because it is more flexible. There is rarely an in-dication to use larger than a 20-gauge needle. If increased in-tracranial pressure is believed to be likely, use as small a needle as possible.

B. Prepare patient Before beginning, examine the fundi to ex-clude papilledema. With an alert patient, explain the proce-dure before beginning in order to diminish the apprehension most patients have about this procedure. The patient does not need to be told every detail of anatomical consideration of a lumbar puncture but rather a simple explanation of the pur-

4 Lumbar Puncture

Fig 1-1.—Sitting (top) and lateral decubitus (bottom) positions used for lumbar puncture.

Technique 5

pose of the procedure and reassurance regarding indications for it, in order to lessen the anxiety and diminish any fearful fantasies regarding a "dangerous attack from the rear." It may be helpful to premedicate an apprehensive patient.

C. Position patient (Fig 1 - 1 ) An assistant should always be available to hold the patient. Place the patient in the lateral decubitus position, preferably on a firm surface. Tuck the pa-tient's knees under the chin and flex the patient's head for-ward as far as possible. The patient should be held in this position by the assistant by placing one hand behind the knees and one hand behind the head. This spinal flexion "opens up" and affords the max imum space between the spinous processes to facilitate passage of the needle. It is important that the pa-tient's back be perpendicular to the floor. A pillow under the patient's knees will help. It is helpful to have good lighting, with the operator seated with the needle at eye level; this is not always feasible on crowded hospital wards, however.

Inter-r\aL fj v e r t e b r a l

Nerve roots C a u d a

e q u i n a

IrAernsL ver-i eh>ral p l e x u s

Fig 1-2.—Topographic and anatomical landmarks of spinal cord, a, in adults, spinal cord ends at either first or second lumbar verte-bra. Puncture must therefore be performed below L-2, preferably at L 3 - 4 or L 4 - 5 interspaces. For proper angulation of needle, note that the lamina of lumbar vertebrae slopes downward and backward. When resistance to needle is encountered at shallow depth, it is lower border of lamina on which it is impinging; if resistance is deep, it is upper border of lamina, b, subdural space is avascular but dura mater is surrounded by rich plexus of anastomosing vessels that, when punctured, are usual cause of bleeding.

Vertebra^, v e i n

D a r a m a t e r

Ar-aicKnoidl

6 Lumbar Puncture

Any interspace below L-2 can be used in an adult. Com-monly, L3-4 or L4-5 is chosen and preferred (Fig 1 -2 ) . Palpate the interspace between two spinous processes (L3-4 or L4-5) closest to a line between the two iliac crests. Mark this point by gentle pressure with the thumbnail or with the blunt end of a pen.

D. Cleanse the point of entry The entire lumbar area should be thoroughly prepared with povidone-iodine, including the skin overlying both iliac crests, so that they may be palpated with sterile gloves before inserting the needle. Don gloves. Then place sterile drapes. Check the point of insertion again. Infiltrate the subcutaneous and part of the interspinous area selected with a local anesthetic.

E. Insert spinal needle Introduce the needle slowly. It should be parallel to the floor, if the patient is in the proper position. If the needle is angled to either the right or left, the attempt will be unsuccessful. The needle is angled cephalad within the midsagittal plane. Some authors have stated that it should be directed toward the umbilicus, but the position of the umbili-cus varies, particularly in obese patients. Others merely direct the needle approximately 30 degrees cephalad from the per-pendicular.

As the needle is introduced, the bevel should be upward; the numbers on the hub will be pointed upward in this position. It has been suggested that with this technique the longitudinal fibers of the ligaments and dura will be spread apart rather than lacerated by the needle, thereby minimizing subsequent fluid leakage and postlumbar puncture headache.

Advance the needle slowly with the stylet in place. Remove the stylet frequently to see if the subarachnoid space has been entered; replace the stylet before advancing again. Lumbar punctures performed without the stylet in place or with ill-filling stylets have been incriminated for the implantation of epidermal fragments into the spinal canal, with subsequent development of the iatrogenic intraspinal epidermoid tumors.

It is helpful to be led by sensation during the puncture. The ligamentum flavum and the dura can usually be identified separately by the resistances they offer to the needle. The sharp, disposable needles now used do not produce a distinct "pop" as they enter the dura. Consequently, one must be care-ful not to advance too far. The ventral epidural space contains an abundant collection of veins that, when punctured, may-lead to a traumatic tap or to a subdural, epidural, or sub-arachnoid hematoma that may result in cauda equina compression (see Fig 1 - 2 )

If CSF cannot be obtained on removing the stylet the second time, shift the position of the needle slightly by rotating the needle, since its point may be obstructed by a nerve root or

Technique 7

film of arachnoid. If fluid still does not appear, then make a second attempt utilizing the adjacent rostral interspace. If this is unsuccessful, make another attempt with the patient sitting and "hunched" over (see Fig 1 -1 ) . However, before measuring the opening pressure, place the patient in the decubitus posi-tion.

If the patient complains of a sharp pain in either leg and if no fluid is obtained, the needle has struck one of the roots of the cauda equina outside the lumbar sac. Withdraw the point of the needle almost to the skin and redirect it. A change in direction cannot be made by shifting the hilt of the needle when the point is deep in tissue.

F. Measure opening pressure When CSF appears in the hub of the needle, advance the needle 1 mm farther so that it is en-tirely within the subdural space, and insert the stopcock with the manometer inserted into the needle. If possible, ask the patient to straighten his legs and relax in order to decrease the intra-abdominal pressure that could lead to an artificial elevation of the opening pressure. If the patient is receiving ventilatory assistance, discontinue the respirator for a few seconds. Then take the opening pressure quickly because the pressure may drop to normal within 1 minute even without withdrawal of fluid. Avoid forced deep breathing to "calm" the patient since the resulting hypocapnia could induce falsely low pressure readings owing to cerebral vasoconstriction. A spontaneous fluctuation of 5 to 15 mm in level of pressure is normal. As a rule, there is a change in fluid pressure of 2 to 5 mm with each heartbeat and of 4 to 10 mm with each respi-ration. There may be falsely reduced pressures when the nee-dle lumen is partially obstructed by tissue fragment or a nerve root. The patency of the needle can be checked by having the assistant apply pressure on the patient's abdomen or by hav-ing the patient cough. If the needle is not patent, the pressure will not rise.

G. Collect fluid specimens After measuring opening pressure, collect specimens by allowing the CSF, including that in the manometer, to drip into three or four specimen containers. Generally, a total of 5 to 10 ml should be taken (1 to 2 ml per tube). If hemorrhagic fluid appears, note carefully whether it clears as more fluid is removed. Even if the opening pressure is high, withdraw a volume of fluid adequate to complete the necessary tests. In patients with increased intracranial pres-sure it is the subsequent leakage through the initial puncture of the dura that is dangerous, not the volume of fluid removed; in general, there will be enough within the manometer for the necessary studies.

H. Remove needle When adequate volume has been collected,

8 Lumbar Puncture

remove the needle and tell the patient to remain supine or prone for several hours. Postlumbar puncture orders to this effect must be written. It is absolutely essential that the si-multaneous blood glucose level is determined.

I. Process fluid samples obtained Send the CSF specimen to the laboratory for blood cell count, differential cell count, and glucose and protein determinations. One may consider order-ing a protein electrophoresis or cytologic study in order to di-agnose MS or malignant neoplasm, respectively. It is always prudent to save one specimen (preferably in a refrigerator) in case the others are lost, and in the event that an additional laboratory examination becomes necessary later. Not infre-quently one of the tubes sent to the laboratory becomes lost or broken, and the possession of the extra tube becomes invalu-able. If meningitis is suspected or if the fluid is cloudy, pre-pare a Gram stain and interpret it immediately. If the initial smear is negative, examine the CSF sediment. A Gram stain, culture (blood agar, chocolate, various broths, and, sometimes, MacConkey's agar are generally used), India ink preparation should be done by the physician or the hospital laboratory. The detection of budding forms of the yeast will help distin-guish cryptococci from lymphocytes, with which they are often confused.

If fluid is hemorrhagic, centrifuge the first and the last tube promptly in order to compare the volume of red blood cells (RBCs) and the clarity of the supernatant fluid in each tube. Bacterial organisms may be seen on the Gram stain even though the CSF fluid is visibly clear. Specific therapy for men-ingitis based on a positive Gram stain should be initiated without delay. A CSF VDRL is very important since the blood VDRL may be negative in cases of neurosyphilis.

IV. COMPLICATIONS In a large series of patients, it was shown that the incidence of postlumbar puncture headache was de-creased from 36.5% to 0.5% by having the patients lie prone for 3 hours. However, in another study, the authors were unable to demonstrate any difference between the prone and supine posi-tions. Generally, however, patients should be asked to remain su-pine or prone for 3 to 6 hours after lumbar puncture. It is often recommended that patients be encouraged to increase their fluid intake in order to facilitate the production of CSF. This is com-monly done, although proof of its efficacy is lacking.

Some complication of lumbar puncture can be elicited by care-ful questioning and evaluations in 75% of patients subjected to lumbar puncture. As a rule, the bulk of these will be minor com-plaints, such as a short period of nonpostural mild headache im-mediately after the puncture, unusual tiredness, slight numb-ness, and insomnia.

Complications 9

A. Headache The most common complication of lumbar punc-ture is headache. It has been reported in 20% to 30% of pa-tients in some series. It is more common in females and pa-tients below 50 years of age. This is postural in nature, ap-pearing with assumption of the erect position and usually re-lieved by recumbency. Its location is variable, but it is usually either occipital or behind the eyes. It is described by the pa-tients as "a constricting band, heaviness, vacuum-like, dead weight, and worse on moving." It is usually associated with nausea in 30% to 40% of the patients and backache in 60% to 70%. The backache lasts 1 to 2 days, is made worse by bend-ing, and is itself rarely severe enough to be incapacitating. It is the headache that in some cases is severe enough to be in-capacitating and in these cases may be associated with vom-iting. As a rule, the onset of headache is within the first 3 days of lumbar puncture, lasts less than 3 to 4 days, and in the vast majority of cases will subside spontaneously, al-though in rare cases it may persist for months. The headache is occasionally (<0.5%) associated with visual (double vision, blurring, photophobia, trouble focusing) or auditory (decreased hearing, plugging, popping, tinnitus, buzzing) symptoms. Less commonly (0.25%) there may be associated cranial nerve dis-turbances, mostly of the sixth or seventh nerve.

The consensus indicates that the postlumbar puncture head-ache is due to leakage of spinal fluid through the needle site in the dura at a rate greater than its production by the choroid plexus, thereby resulting in a reduced circulating CSF vol-ume. This reduced volume is thought to result in loss of buoy-ancy, thereby permitting the downward shift of the brain in the upright posture. This stretches the pain-innervated basal meninges and pain-sensitive blood vessels that Signal the headache.

The most important factor in the postlumbar puncture headache is the size of the needle used. The use of smaller needles substantially decreases the incidence of headache. Other contributing factors are the position and state of hydra-tion of the patient.

B. Herniation The major complication of lumbar puncture is herniation of the brain through the tentorium or foramen magnum in patients with increased intracranial pressure. The data in the literature are inconclusive concerning the magni-tude of this risk. One group showed that only 1.2% of 418 pa-tients with papilledema had this complication from lumbar puncture. Another group of authors reported only one such complication of lumbar puncture in 401 patients with docu-mented brain tumors. One widely quoted study reports 30 cases in which the condition of patients with increased intra-cranial pressure deteriorated within 12 hours after lumbar

10 Lumbar Puncture

puncture. Forty-seven percent of these patients died and an-other 14% were severely disabled. Unfortunately, the author does not state what percentage of the patients at risk is rep-resented in this group. It is generally accepted that a patient with papilledema or a clinical syndrome suggestive of a mass lesion has a substantial risk of this complication. Of the 30 patients mentioned above, about three fourths had focal or lo-calizing neurologic signs at the time the lumbar puncture was performed and 30% had papilledema. In patients with brain abscesses, lumbar punctures are associated with a high risk (8% to 29%) of related neurologic complications. Moreover, lumbar puncture is usually unrewarding or misleading in the diagnosis of suspected brain abscess in the absence of menin-gitis. Consequently, when brain abscess is suspected, lumbar puncture should be withheld until more definitive studies can be performed (computed axial tomography, angiography).

C. Hematomas In the past several years, numerous cases of subdural, epidural, or subarachnoid hematomas leading to compression of the cauda equina have been reported as com-plications of lumbar puncture. Presumably, this is a result of trauma to the ventral or dorsal venous plexus and it has been reported even in the absence of RBCs in the CSF. Almost all of these cases have been reported in patients who were either anticoagulated or thrombocytopenic. There have been at least two cases reported in which this complication occurred after repeated lumbar puncture in the absence of any evidence sug-gesting clotting abnormality. Clinically, these patients have rapidly developing flaccid paraplegia (generally within 24 hours), sensory loss in the lower extremities, and urinary re-tention. Consequently, in patients with a clotting abnormality or thrombocytopenia, lumbar puncture should be performed only for the most compelling reasons. The smallest possible needle should be used and the procedure should be performed only after every possible therapeutic maneuver has been uti-lized to reduce the bleeding risk (i.e., platelet transfusion, re-versal of warfarin sodium or heparin anticoagulation, or factor replacement). The most skillful available physician should perform the procedure and the patient should be followed up carefully afterward.

D. Miscellaneous Other rare complications of lumbar puncture are iatrogenic meningitis (Candida, staphylococci, and Pseu-domonas have been reported as etiologic agents), intradural epidermoid tumors, and spinal-cutaneous fistulas.

V. INTERPRETATION (Table 1 -1 )

A. The normal opening pressure ranges from 130 to 200 mm H20. It is increased with cough, strain, tumors, hematomas,

Interpretation 11

abscesses, and infections. Low pressures are encountered mostly in volume-depleted patients.

B. CSF fluid appearance The CSF fluid itself should be clear. A turbid appearance correlates with at least 500 cells per cubic millimeter. Turbidity is sometimes also seen with a very high protein content, as in situations with brain necrosis. Xan-thochromia may be seen from 2 to 18 hours following intracra-nial bleeding. A protein level of greater than 150 mg/dl may also give the fluid a xanthochromic color. Grossly bloody fluid suggests a subarachnoid hemorrhage or traumatic tap.

C. White blood cells (WBCs) Normal CSF contains a maximum of 3 to 5 WBCs, all of which should be lymphocytes. The pres-ence of even one polymorphonuclear leukocyte should proba-bly be considered abnormal and an explanation for its pres-ence sought. In aseptic meningitis, the cell count is usually below 1,000/cu mm and consists mainly of mononuclear cells. Early in aseptic meningitis, there may be a predominance of polymorphonuclear leukocytes. In bacterial meningitis the cell count is usually greater than 500 WBCs per cubic millimeter and consists predominantly of polymorphonuclear leukocytes. Early bacterial meningitis may be diagnosed by a positive Gram stain without the presence of any WBCs. However, pre-cipitated stain being misinterpreted as gram-positive cocci is one of the most common errors made on CSF Gram stains. Large mononuclear cells of meningeal carcinomatosis may be seen in some patients.

D. The CSF protein level is normally between 15 to 45 mg/dl. It is greater than this in 90% of cases of bacterial meningitis and usually ranges between 100 to 500 mg/dl. Elevated CSF protein levels may also be seen in aseptic meningitis, toxic encephalopathy, chronic phenothiazine ingestion, diabetes mellitus (increased CSF protein levels are present in at least 80% of diabetic patients who have peripheral neuropathy), Guillain-Barre syndrome, neoplasms, syphilis, cerebrovascu-lar accidents, and in some uremic patients. The CSF protein level may be elevated in polyneuropathy, a finding that differ-entiates polyneuropathy from other conditions producing weakness. Protein electrophoresis is of value in the diagnosis of MS, though the -/-globulin level is also elevated in syphilis and connective tissue disease.

E. The CSF glucose level is usually greater than half of a si-multaneous blood glucose level. Low CSF glucose level is seen with acute bacterial meningitis, some viral meningitis (mumps, herpes simplex, and lymphocytic choriomeningitis), and tuberculous, fungal, carcinomatous, or sarcoid meningitis.

F. Traumatic lumbar puncture Occasionally a problem arises in

12 Lumbar Puncture

Table 1 - 1 CSF CHARACTERISTICS

WBCs

APPEARANCE PRESSURE

(Mm H,0) CELL COUNT

WBCs/cu Mm) PREDOMINANT

CELL TYPE*

Normal Bacterial

meningitis Tuberculous

meningitis Aseptic or viral

meningitis

Fungal meningitis

Brain abscess

Asymptomatic neurosyphilis

Meningovascular syphilis

Brain tumor

Clear Cloudy,

purulent Cloudy

Clear or cloudy

Clear or slightly cloudy

Clear

Clear

Clear or slightly cloudy

Clear

70-200 300-1,000

200-500

Normal or slightly elevated

>200 225-500t

200-300

Normal or slightly elevated

Normal

200 -800

<5 >100 500-20,000+ >25 100-500t 5-100 <l,000t

20-1,000

M PMN

Early, PMNs; in 7 - 1 4 days, M

M (very early,

PMNs) M

May be normal <200t

Normal or >25 but <500t

6 - 1 0 0

0 - 2 0 0

M (rarely PMNs)

M

M

M

*M indicates mononuclear cells; PMN, polymorphonuclear leukocytes, tlndicates the range: minimum and maximum. tPositive if no prior antibiotic therapy. Negative in partially treated meningitis.

determining a significant number of WBCs and elevation of protein level in the setting of a traumatic lumbar puncture. In general, one can expect one WBC per 750 to 1,000 RBCs in a traumatic tap. One may expect the CSF protein level to be elevated 1 mg/dl per 750 to 1,000 RBCs.

G. Differentiation of subarachnoid hemorrhage from traumatic lumbar puncture Subarachnoid hemorrhage is often associ-ated with an increased opening pressure, xanthochromic su-pernate after the fluid is centrifuged, and a uniform hemato-crit reading in various tubes. A traumatic tap is associated with normal and low pressure, a clear supernate, and gradual decrease in the number of RBCs or hematocrit reading in suc-cessive tubes (always compare the first tube with the last).

The supernate should be water-clear if RBCs have been pre-sent for less than 2 hours. One clinical axiom has it that if the

Interpretation 13

GLUCOSE COMMENTS AND

SPECIFIC FINDING

PROTEIN (Mg/Dl)

COMPARED CONCENTRATION TO BLOOD

(Mg/Dl) GLUCOSE (%) STAIN CULTURE

15-45 100-500

5 0 - 2 0 0

45-100

25-100 (rarely, up

to 500) 45-100

>45

50-100 <50

<50

50-100

<50

50-100

50-100

50-65 <40

<50

>50

<50

>50

>50

Negative Positive t in Positive i in

70%-80% Positive in

10% Negative

85%-Positive in

40%-90% Viral may

be positive

Budding yeast Fungal

Negative Negative

VDRL positive

45-200 50-100 >50 VDRL positive

20-500 Normal, decreased in carcinomatous meningitis Cell block positive

ward clerk can pick the tube of CSF from another containing water, the fluid is not clear and intrinsic bleeding should be considered. Jaundice and a protein content of over 150 mg/dl can give a xanthochromic appearance. Crenated RBCs are of no consequence. Supernatant fluid may be sl ightly xantho-chromic if a traumatic bloody tap contains over 100,000 RBCs per cubic millimeter, sufficient serum having accompanied the blood to give a yellow tint. Such gross bleeding is rare; when present, it is accompanied by enough fibrinogen to produce a clot in the tube.

H. The detection of bacterial antigens in the CSF by countercur-rent immunoelectrophoresis is a highly reliable and rapid di-agnostic test of bacterial meningitedes caused by Streptococ-cus pneumoniae, Neisseria meningitidis, or Hemophilus in-fluenzae.

14 Lumbar Puncture

REFERENCES

Lee J.A., Atkinson R.S.: Sir Robert Mackintosh's Lumbar Puncture and Spinal Analgesia, ed. 4. New York, Churchill Livingstone, Inc., 1978.

This monograph written for the anesthesiologist is profusely and beautifully illustrated with careful anatomical dissections of the vertebral column. The chapter on the technique of lumbar puncture is one of the most thorough on the topic.

Dawson H.: Physiology of the Cerebrospinal Fluid. Boston, Little, Brown & Co., 1967.

This extensive monograph tells you most (but not all) of what you may want to know about the physiology of the CSF.

Petito F., Plum F.: The lumbar puncture. N. Engl. J. Med. 290:225-227, 1974.

A well-written editorial summary of the technique of lumbar punc-ture.

Best techniques (several) for lumbar puncture, letters to the editor. N. Engl. J. Med. 290:1260-1262, 1974.

Three interesting letters narrating each author's experience and preferred technique of lumbar puncture.

Tourtellotte W.W., Henderson W.G., Tucker R.P., et al.: A random-ized, double-blind clinical trial comparing the 22- vs 26-gauge needle in the production of the post-lumbar puncture syndrome in normal individuals. Headache 12:73-78, 1972.

A careful, detailed, follow-up study presenting convincing evidence for the role of needle size in the development of postpuncture symp-toms. The use of the 26-gauge needle will reduce, on the average, the number of patients who suffer a postural headache from one out of every three (36%) to one out of every nine (12%) subjects punc-tured. The incidence of nausea is also reduced from 72% to 33% and that of backache from 72% to 56%. Symptoms are more fre-quent in females (40%) than males (13%). The drawbacks of the smaller needle are (1) difficulty in manipu-lating the tip into a position where it is not intermittently obstructed by nerve root filaments and (2) the slower rate of fluid withdrawal.

Lundberg N., West K.A.: Leakage as a source of error in measure-ment of the cerebrospinal fluid pressure by lumbar puncture. Acta Neurol. Scand. 41(suppl. 13):115-121, 1965.

Leakage of fluid around the needle may cause considerable decrease in CSF pressure after lumbar puncture, particularly in patients with pronounced intracranial hypertension who are punctured with large-bore needles. In ten neurosurgical patients whose ventricular fluid pressure was being continuously monitored, a substantial drop in ventricular fluid pressure occurred in five cases after lumbar puncture without removal of fluid. All five had increased fluid pressure. The time between insertion of needle and fall in pressure was 1 to 3.5 min-utes.

References 15

Korein J., Cravioto H., Leicach M.: Re-evaluation of lumbar punc-ture: A study of 129 patients with papilledema or intracranial hy-pertension. Neurology 9:290-297, 1959.

Lumbar puncture was performed in 70 patients with papilledema and 59 with increased CSF but without edema. A review of similar studies in the literature of 1,053 other such cases tabulated. Actual complications of careful diagnostic puncture in the presence of pap-illedema is calculated to be less than 1.2%.

Lubic L.G., Marotta J.T.: Brain tumor and lumbar puncture. Arch. Neurol. Psychiatry 72:569-572, 1954.

A review of the postmortem findings in a series of 40 patients with histologically verified brain tumor in whom lumbar puncture had been performed. Papilledema and increased pressure were present in one third of the cases. Only one case showed evidence indicating an untoward effect of lumbar puncture: possible uncal herniation.

Duffy G.P.: Lumbar puncture in the presence of raised intracranial pressure. Br. Med. J. 1:407-409, 1969.

Probably the most damning evidence against lumbar puncture in the presence of increased intracranial pressure. A study of 30 pa-tients with increased intracranial pressure, one third of whom had papilledema. Following lumbar puncture there was a dramatic de-terioration in the patient's condition either immediately (50%) or within 12 hours of puncture (50%), with an overall mortality of 40% within 10 days of puncture.

Carey M.E., Chou S.N., French L.A.: Experience with brain ab-scesses. J. Neurosurg. 36:1—9, 1972.

A study of 86 patients with brain abscess. Lumbar puncture as a diagnostic tool was inaccurate (normal in one third) and occasion-ally fatal. It was implied as cause of death in six patients who her-niated within 12 to 36 hours of puncture.

Garfield J.: Management of supratentorial intracranial abscess: A review of 200 cases. Br. Med. J. 2:7-11, 1969.

The hazards of lumbar puncture are real. In 41 of the 140 patients who underwent lumbar puncture, there was a substantial deterio-ration in the level of consciousness during the subsequent 48 hours. Eleven of the patients whose conditions deteriorated after lumbar puncture were either fully alert or mildly drowsy, and only two had papilledema.

Edelson R.N., Chernik N.L., Tosner J.B.: Spinal subdural hemato-mas complicating lumbar puncture occurrence in thrombocytopenic patients. Arch. Neurol. 31:134-137, 1974.

Eight patients with thrombocytopenia (3,000 to 73,000 platelets/ ml) of various causes (leukemia, idiopathic thrombocytopenic pur-pura) developed spinal subdural hematomas following lumbar puncture. In three, the hematoma was associated with weakness and sensory loss in the lower extremity as well as bladder dysfunc-tion. One of these patients recovered spontaneously, while the other two remained paraplegic.

Messer H.D., Forshan V.R., Brust J.C.M., et al.: Transient paraple-

16 Lumbar Puncture

gia from hematoma after lumbar puncture: A consequence of anti-coagulant therapy. JA.MA. 235:529-530, 1976.

In patients who are to be anticoagulated and who may require a lumbar puncture, tap before anticoagulation. A 51-year-old man receiving heparin for a transient ischemic attack developed flaccid paralysis and bladder atony 3 days following lumbar puncture. He recovered 10 days later.

Rengarchary S.S., Murphy D.: Subarachnoid hematoma following lumbar puncture causing compression of the cauda equina. J. Neu-rosurg. 41:252-254, 1974.

Blood in the subarachnoid space does not usually clot, probably because of dilution by CSF, except if bleeding is massive and rapid. A 64-year-old man developed flaccid paralysis in the legs and uri-nary retention 12 hours after spinal anesthesia. Laminectomy done to evaluate the clot resulted in 60% recovery of function over 4 weeks, with no further subsequent improvement.

Dripps R.D., Vandam L.D.: Hazards of lumbar puncture. JA.MA. 147:1118-1121, 1951.

While intended for the anesthesiologist, this is a well-written sum-mary of some of the complications of lumbar puncture.

Vandam L.D., Dripps R.D.: Long-term follow-up of patients who re-ceived 10,098 spinal anesthetics: Syndrome of decreased intracranial pressure (headache and ocular and auditory difficulties). JA.MA. 161:586-591, 1956.

The overall incidence of headache was 11%. The oldest patients (>50 years) were less susceptible than women (14%). The most im-portant variable is the size of needle used, with the incidence of headache being 18% with 16-gauge needles, 14% with 20-gauge, 9% with 22-gauge, and 6% with 24-gauge.

Brocker R.J.: Technique to avoid spinal-tap headache. JA.MA. 168:261-263, 1958.

Rather dramatic evidence for having the patient lie prone for 3 hours after puncture. Following lumbar puncture in a group of 1,094 patients, 894 patients were placed prone on their abdomen for 3 hours while the other 200 were kept supine in bed. The inci-dence of postlumbar puncture headache was 0.5% in the first group as compared to 36.5% in the second group!

Tourtellotte W.W., Haerer A.F., Hiller G.L., et al.: Postlumbar Puncture Headaches. Springfield, 111., Charles C Thomas, Publisher 1964.

An extensive review of the topic. Bullard J.R., Alpert C.C., Woerth S.D.: Postlumbar puncture head-ache: A review of the literature. J. S.C. Med. Assoc. 24:179-181, 1978.

Contrary to its title, this is not an extensive review of postlumbar puncture headache, but rather a good summation of what is known about it.

Kadrie H., Driedger A.A., Mclnnis W.: Persistent dural cerebrospi-

References 17

n a l fluid leak shown by retrograde radionuclide myelography. J. Nucl. Med. 17:797-799, 1976.

Convincing pictorial documentation of CSF leak following lumbar puncture as the cause of the postlumbar puncture headache. Evi-dence is presented for the efficacy of "blood-patch technique" in re-pairing persistent dural leak.

Brodsky J.B.: Epidural blood patch: A safe, effective treatment for post-lumbar puncture headache. West. J. Med. 129:85-87 , 1978.

A good review of the epidural blood-patch technique used by anes-thesiologists since 1970 in the management of incapacitating post-lumbar puncture headache: 2 to 3 ml of a patient's blood injected at the site of dural puncture forms a gelatinous tamponade that seals the leakage site. One danger is nerve root pain and pares-thesia.

Branitzky S., Keucher T.R., Mealey J., et al.: Iatrogenic intraspinal epidermoid tumor. JA.M.A. 237:148-150 , 1977.

Intraspinal epidermoid tumors result from the implantation of skin fragments within the spinal canal by the lumbar puncture needle. These tumors are manifested with progressive back and leg pain, 1.5 to 23 years after lumbar puncture.

Lombardi G., Passerini A.: Spinal Cord Diseases: A Radiographic and Myelographic Analysis. Baltimore, Will iams & Wilkins Co., 1964, p. 160.

Epidural, subdural, and subarachnoid hematomas may occur af-ter repeated lumbar puncture even in the absence of clotting defects.

Redlich F.C., Moore B.E., Kimbell I.: Lumbar puncture reactions: Relative importance of physiological and psychological factors. Psy-chosom. Med. 8 :386-398 , 1946.

A revealing study of the postlumbar puncture unfavorable reactions in 100 psychiatric patients punctured routinely. Before the punc-ture, half of the patients had heard of someone who had undergone the test and 23% knew of ill effects. There was some increase in mild reactions associated with the anticipatory anxiety present in the latter group. Occurrence of symptoms had no significant rela-tionship to intelligence and emotional stability. Persons with nor-mal mood seemed to suffer more severe headache than those who were depressed or elated. The presence of chronic anxiety or hypo-chondriasis predisposed to a slight increase of complications, but not of severe reactions.

Soskolne E.I., Kuhn S.H., Van Der Merwe P.L., et al.: The need to repeat lumbar puncture. S. Afr. Med. J. 51:395-396 , 1977.

In the presence of clinically suspected meningitis with obvious men-ingeal signs and symptoms, a normal specimen of CSF does not exclude meningitis. The initial tap may be normal in bacterial men-ingitis.

Feigin R.D., Shackleford P.: Value of repeat lumbar punctures in the differential diagnosis of meningit is . N. Engl. J. Med. 289:571-574 , 1973.

18 Lumbar Puncture

In aseptic or viral meningitis, the "early" spinal fluid may reveal a preponderance of polymorphonuclear leukocytes. The clue is a nor-mal glucose level of the fluid. A second tap 12 hours later will re-veal a preponderance of lymphocytes in aseptic meningitis.

Aloia J.F., Esswein A.J., Weissman M.B.: Housestaff performance of the lumbar puncture as a measure of clinical skills teaching. J. Med. Educ. 52:689-690, 1977.

A study of 18 level 1 house officers at the end of their 6 months of training observed at the bedside while performing lumbar punc-tures and rated on 36 items of technique abstracted from the Amer-ican College of Physicians' Skill Library and incorporated into a checklist form. Of a total of 620 items rated, there were 124 errors! It is obviously of concern that errors observed in these interns would be transmitted to medical clerks and eventually to the following year's level 1 trainees.

19

Thoracentesis

I. INDICATIONS

A. Pleural effusion of unknown cause Specific studies on fluid may be helpful in determining causes of effusion.

B. Relief of dyspnea secondary to large amount of pleural fluid When due to congestive heart failure, thoracentesis may result in sufficient improvement of cardiopulmonary function to prevent the recurrence of the effusion.

C. Pleural biopsy (see chapter 3).

D. Emergency tension pneumothorax Thoracentesis, usually performed in the anterior second intercostal interspace, can be lifesaving.

E. Instillation of medications Examples: sclerosing agents in recurrent effusions or pneumothoraces and antineoplastic agents for tumors.

F. Documentation of presence of effusion when chest roentgen-ograms, including lateral decubitus films, are equivocal.

II. CONTRAINDICATIONS

A. Clinically significant bleeding disorders (unless procedure is an emergency) An attempt should be made to correct the clotting disorder prior to the thoracentesis. In the patient re-ceiving intravenous heparin, thoracentesis can usually be done 4 to 6 hours after the-last dose. In the patient receiving subcutaneous heparin, thoracentesis can be performed just prior to the next scheduled dose.

B. Uncooperative patient Cooperation in keeping a stationary position is essential to performing a safe thoracentesis.

C. Uncontrollable hiccups or coughing To avoid puncture or tear of the lung by the needle, hiccups or cough must be con-trolled before thoracentesis. Prior to the start of the procedure,

1 9

20 Thoracentesis

instruct the patient to withhold from coughing while the nee-dle is in the chest cavity and to inform the physician if this becomes impossible.

III. TECHNIQUE

A. Assemble proper equipment Sponges and preparatory solu-tion, sterile gloves, sterile towels, local anesthetic, 25- and 20-gauge needles, 7.5-cm thoracentesis needle, a 30- or 50-ml and two 10-ml syringes, a three-way stopcock, 37.5-cm sterile tub-ing, hemostat, sterile fluid-collection containers (basin, vac-uum bottle, tubes, etc.), and adhesive dressing will be needed.

B. Locate level of fluid, both by physical examination and by roentgenogram.

C. Position of the patient may vary depending on the indication and the amount and location of fluid present. For fluid re-moval the most common and effective approach is the poste-rior one (Fig 2 - 1 ) . The patient sits on the side of the bed,

Fig 2-1.—Posit ion of patient for thoracentesis. Inset, proper en-try route of needle: just above lower rib of selected interspace to avoid vasculature traversing inferior margin of rib above intercostal space being penetrated.

Technique 21

leaning forward, the arms abducted with the head and arms supported by a pillow on the bedside adjustable table. The puncture site will be along the posterior axillary line. Alter-natively the patient may lie supine in bed, with the head of the bed elevated at 60 degrees and the arm, on the side to be tapped, held over the head. With this approach the site of the puncture will be along the midaxillary line. This position can be used for isolated anterior collections on the right side with the puncture site along the midclavicular line.

D. The puncture site is usually below the fluid level. A puncture site that is too low may result in penetration of subdiaphrag-matic organs. This can be avoided if the puncture site is above the ninth rib posteriorly, the seventh rib laterally, and the fifth rib anteriorly. As a rule, the space between the seventh and eighth ribs or the eighth and ninth ribs is used with the posterior approach (see Fig 2 -1 ) .

E. Maintain strict aseptic technique Clean a large area around the selected puncture site (10 to 12.5 cm in diameter) thor-oughly with an antiseptic solution. Apply sterile drapes below the thoracentesis site and on the adjacent bed space, which can then be used as a convenient working area. Drapes placed above the puncture site can prove to be a nuisance, as they have a tendency to fall down at a most critical time during the procedure. In hirsute males, shaving the area around the site may be necessary. In the long-haired female, putting a surgical cap to hold the hair up not only ensures the sterility of the field but also saves considerable aggravation during the procedure.

F. Anesthetize skin and pleura Only the skin and parietal pleura are sensitive, and it is not necessary to infiltrate the whole thickness of the chest. About 0.5 to 1 ml should be suf-ficient to anesthetize the former and 3 to 5 ml the latter. Anesthetize the skin with a 25-gauge needle. Then use a 20-gauge needle for deeper infiltration. It is very important to remember that the intercostal nerve and blood vessels are lo-cated just beneath each rib (see Fig 2 - 1 , inset). Always ad-vance the needle above the lower rib; do not get close to the inferior margin of the rib above the intercostal space being penetrated. In the obese patient, the rib location may be de-termined by the needle tip. When the advancing needle strikes the rib, it is redirected along a path over the rib mar-gin, thereby avoiding the intercostal neurovascular bundle. When the needle touches the parietal pleura the patient will usually complain of pain. Following gentle aspiration to rule out vascular injury, the pleura is now thoroughly anesthe-tized.

G. Advance the needle with gentle suction, through the anesthe-

22 Thoracentesis

tized path, until pleural fluid appears. Then remove the nee-dle, after carefully noting the depth to which the thoracentesis needle will have to be inserted to reach the pleural field.

H. Obtain pleural fluid Attach a long 17- or 18-gauge needle to a 30- to 50-ml syringe via a three-way stopcock that is con-nected to the drainage tube. The operator should familiarize himself with the mechanics of this assembly and ascertain the snugness of its connections. Now advance the thoracentesis needle with constant gentle aspiration along the path of the anesthetic needle and to the same depth. A small superficial incision of the skin with a No. 11 blade will make the entry of this larger needle easier. Remember, the needle should be ad-vanced above the lower rib. When pleural fluid is obtained, place a hemostat on the needle at the skin level to prevent it from inadvertently slipping forward.

I. Remove the desired amount of fluid through the tube into the collecting system. A catheter (14-gauge Intracath) can be used to drain large amounts of pleural fluid. This will prevent injury or tear of the lung by the needle bevel and will permit more flexibility; therefore the procedure is less strenuous for the operator. Its disadvantages are slower drainage, plugging with fibrin, difficulty of directing the catheter tip with any accuracy, and occasional loss of the catheter into the pleural space.

J. Remove needle and seal puncture After the procedure is completed, remove the needle and apply finger pressure im-mediately to the puncture site to seal the puncture and pre-vent aspiration of air into the pleural space. Place a Band-Aid over the wound.

K. Process fluid samples Fluid obtained may be sent for cell count and differential cell count; glucose, protein, lactic dehy-drogenase (LDH), and amylase determinations; rheumatoid factor and complement analysis; Gram and acid-fast stain; bacterial tuberculous and fungal cultures; cytologic study; cell block; or pH as indicated. Heparin or ethylenediamine tetra-acetic acid (EDTA) may be necessary to prevent clotting in transfer tubes.

L. Follow-up After the procedure, check the vital signs fre-quently for a brief period of time and inspect the puncture site for bleeding. Obtain a chest roentgenogram immediately after thoracentesis and review it for pneumothorax.

IV. COMPLICATIONS

A. Pneumothorax This is the most common complication of thoracentesis. In general, these are small in volume, clinically

Complications 23

inconsequential, produce no symptoms, and are noted as an air-fluid level on the postthoracentesis chest films. If larger in volume, the patient becomes more dyspneic during the proce-dure, in which case as much air as possible should be aspi-rated and a tube should be placed in the chest and connected to an underwater-seal drain.

B. Hemorrhage Bleeding may be caused by penetration into the lung parenchyma or damage of an intercostal artery. The for-mer can be recognized by the aspiration of frothy blood or bloody return after an initially serous drainage and may be associated with hemoptysis. This is usually not serious and is common when there is only a small amount of fluid. Bleeding from an intercostal artery can be recognized by obtaining in-creasingly bloody fluid from the outset of thoracentesis. It can be avoided by introducing the needle superior rather than in-ferior to a rib margin.

In either case, the patient should be closely observed after the procedure for occult bleeding by serial hematocrit readings and for hemothorax or increasing fluid accumulation by chest roentgenograms.

C. Vasovagal episode Not infrequently, an anxiety attack characterized by palpitation, difficulty in breathing, tightness in the throat, sweating, trembling, and giddiness will occur either during the procedure or immediately following it.

D. Infection Strict aseptic technique is essential throughout the thoracentesis in order to avoid introducing an infection. The spread of infection by the inadvertent aspiration of a pulmo-nary abscess is rare; it can be avoided by prior accurate local-ization of the fluid collection.

E. Pulmonary edema Unilateral pulmonary edema may de-velop when a large collection of fluid or air is drained from the pleural cavity. The edema develops in the lung that had been compressed chronically (weeks to months) and only if over 1,000 ml of fluid is removed. It can be suspected by the onset of coughing and tightness in the chest during the procedure. It can be avoided by limiting the volume of aspiration to 500 to 1,000 ml if pleural effusion has been present for over a week and to less than 1,500 ml in any circumstance.

F. Puncture of parapleural viscera occurs when diseases of the liver or spleen (hepatic abscess, subdiaphragmatic abscess) cause an abnormal elevation of the diaphragm, or when the needle insertion is too low. A thorough physical examination and a recent chest film to localize the diaphragm and proper selection of the interspace to penetrate should avoid this com-plication.

G. Subcutaneous emphysema will form around the needle entry

24 Thoracentesis

site, particularly when larger-bore needles are used and no pressure is applied to seal the puncture immediately after re-moval of the needle.

H. Hypoxemia Some degree of hypoxemia may occur soon (20 minutes to 2 hours) after drainage of pleural effusion. Respi-ratory embarrassment may then ensue in patients with com-promised cardiopulmonary function. The degree of hypoxemia is directly related to the volume of fluid removed and is prob-ably due to increased blood flow through the atelectatic seg-ments as the lung expands to replace the fluid removed. This is a self-limited complication that subsides in 12 to 24 hours and can be prevented by supplemental oxygen therapy follow-ing the thoracentesis.

I. Air embolism or "pleural shock" is a rare but dramatic com-plication caused by the inadvertent penetration of a pulmo-nary vein. It is most likely to occur with a pneumothorax pro-cedure when the lung expands against the needle bevel as the air is being evacuated. It is a potentially fatal complication characterized by dyspnea and abnormal CNS manifestations (visual, convulsive, and consciousness).

J. Protein depletion is a potential risk in the patient in need of constant drainage or undergoing repeated thoracentesis.

V. INTERPRETATION Pleural effusions often present the earliest evidence of an underlying disease. Examination of the fluid ob-tained by thoracentesis may be the most efficacious means of identifying the underlying disease. Even when the cause of the effusion is clinically obvious, the pleural fluid, once obtained, should be investigated, not only to confirm the diagnosis but also to rule out the unsuspected presence of a potentially serious but treatable disease occurring either de novo (cancer in an elderly patient in congestive heart failure) or as a complication of the primary disease (infection in the patient with systemic lupus er-ythematosus).

The first step in the evaluation of the pleural effusion is its classification as either an exudate or a transudate. A transudate occurs when the mechanical factors involved with the formation or reabsorption of fluid are altered, such as elevation of the hy-drostatic pressure or reduction of the oncotic pressure (congestive heart failure, hypoalbuminemia, cirrhosis of the liver, nephrotic syndrome). An exudate results when there is pleural inflamma-tion or disease with the consequent leakage of the fluid from the affected vasculature or obstruction of the lymphatic drainage (tu-berculosis, cancer, lymphoma, infection, connective tissue dis-ease, pulmonary infarction). As a rule, the presence of an exuda-tive effusion reflects on the seriousness of the underlying disease

Interpretation 25

and necessitates further diagnostic procedures to establish a de-finitive diagnosis.

Initially, pleural fluid was classified as a transudate when the specific gravity was below 1.016 or when the protein concentra-tion was less than 3.0 gm/dl. The separation of transudates from exudates by these criteria alone is fraught with a 10% to 15% error. The accuracy of the separation is considerably enhanced if measurements of pleural fluid and serum concentrations of pro-tein and LDH are performed simultaneously and the following criteria are applied for an exudate:

1. Pleural fluid to serum protein ratio of greater than 0.5. 2. Pleural fluid to serum LDH ratio of greater than 0.6. 3. Pleural fluid LDH level of over 200 IU/dl or greater than two

thirds the upper limit of normal serum LDH level. The separtion of a transudate from an exudate does not permit

the etiologic classification of pleural effusions. On the other hand, certain other features of the fluid are usually characteristic of specific conditions and may provide a diagnostic clue to the un-derlying disease. In examining the fluid further, it is important to always keep in mind that with most of these other features there is an overlap of values that makes total reliance on them a source of diagnostic error.

A. General appearance Most pleural fluids are clear and light straw-colored. It is the presence of WBCs that imparts the cloudy, turbid appearance seen with exudates containing more than 1,000 WBCs per cubic millimeter. A viscid and opaque fluid indicates a much higher WBC content, characteristic of an empyema. In some of these, the viscosity of the purulent material may be high enough to prevent its drainage with a standard needle. A feculent odor is indicative of an aerobic organism as the cause of the empyema.

When the fluid is blood-tinged, it contains at least 5,000 RBCs per cubic millimeter. The traumatic leakage of 1 ml of blood into 1,000 ml of pleural fluid will result in blood-tinged fluid. As a rule, blood at the beginning or end of a tap indi-cates trauma, whereas truly hemorrhagic effusions remain uniformly bloody throughout the procedure. The prior pres-ence of blood in the pleural fluid can be determined from a Wright stain of the sediment. The presence of pink-staining hemoglobin in the macrophages indicates a hemorrhagic effu-sion. In the absence of history of chest trauma, hemorrhagic pleural effusion (RBCs > 100,000/cu mm or fluid hematocrit reading of 1% to 2%) implies an exudate and is sufficient rea-son to pursue the evaluation of pulmonary infarction or malig-nancy. It is very rare for tuberculosis to cause hemorrhagic effusions.

A milky or golden-yellow fluid suggests chylothorax or cho-lesterol (chyliform) effusion, although the latter is said to

36 Thoracentesis

have a characteristic satin sheen. The two can be quickly dif-ferentiated by obtaining a Sudan III stain for fat globules; mi-croscopy for cholesterol crystals; or the addition of ether, which dissolves triglycerides and clears the opalescence but has no effect on cholesterol. This can be subsequently con-firmed by the determination of lipid (>400 mg/dl) and choles-terol (>145 mg/dl) levels in the fluid. Chylothorax suggests thoracic duct involvement by a tumor, usually a lymphoma. Cholesterol suggests the presence of long-standing effusion as with tuberculosis or rheumatoid arthritis. Rheumatoid effu-sions are classically turbid and greenish-yellow.

B. Specific gravity Extensively used in the past for the separa-tion of an exudate (>1.016) from a transudate (<1.016) the specific gravity test is of limited usefulness today except when a quick answer is needed or when the laboratory is unavail-able. In such instances, the specific gravity must be measured immediately. The chief cause of error in its measurement with a hydrometer is the temperature of the fluid, which may change the specific gravity by as much as 0.008 to 0.010. Re-member that the commercially available refractrometers are calibrated for urine and cannot be used for pleural fluid. How-ever, it has been estimated that a reading of 0.020 on the re-fractometer corresponds to a pleural fluid protein content of 3 gm/dl, and that each deviation of 0.004 from it represents 1 gm protein per deciliter.

C. Protein Protein levels are by far the best means of differen-tiating a transudate from an exudate, particularly when si-multaneous blood levels are obtained. Long-term diuretic therapy, particularly with the currently available potent di-uretics, will increase pleural fluid protein content (sometimes to > 3 gm/dl) because of the more rapid mobilization of water and electrolytes. In the hypoalbuminemic patient (nephrotic syndrome, liver cirrhosis), this may well result in a fluid to plasma ratio of more than 0.5. A high protein content suggests rheumatoid arthritis (>4 gm/dl) or tuberculosis and malig-nancy (>6 gm/dl).

D. LDH When coupled with serum measurement, a pleural fluid to serum ratio of more than 0.6 indicates a transudate. An elevated LDH level but not protein level suggests a malig-nancy. However, it is not uncommon in intrathoracic malig-nancies to obtain pleural fluid with low protein and LDH lev-els, i.e., a transudate secondary to venous obstruction by the tumor.

E. Glucose The glucose content of pleural fluids parallels that of blood. As a rule, the importance of a low pleural fluid glu-cose level is not that it is diagnostic but that it implies pri-mary pleural disease, demanding further investigation. The

Interpretation 27

pleural fluid glucose level is only moderately low in tubercu-losis; it is sometimes (15%) low in neoplastic effusions but in general is greater than 25 mg/dl; it is commonly very low (<10 to 30 mg/dl) in rheumatoid arthritis (85%) as well as collagen diseases and complicated parapneumonic effusions.

F. Amylase The pleural effusion of pancreatitis is usually left-sided, small in volume, and hemorrhagic, with a high amylase content and a fluid to plasma amylase ratio of over 1.0. It may also be elevated in neoplastic effusions and rupture of the esophagus (salivary amylase), but the fluid to plasma ratio will be less than 1.0.

G. pH The pH of the pleural fluid correlates closely with the arterial blood pH. Its interpretation requires the simultaneous measurement of the blood pH and careful handling of the specimen, i.e., as with blood, the sample must be obtained an-aerobically in a heparinized syringe, immediately capped, and kept on ice until the measurement is obtained. In general, the pH is low in inflammatory pleural effusions and normal in neoplastic effusions and transudates. It is very low (<5) with rupture of the esophagus. The main value of pleural fluid pH appears to be prognostic rather than discriminatory. Essen-tially, parapneumonic effusions with a pH less than 7.2 do not respond to antibiotic therapy and will require tube drainage.

H. Cell count and differential The majority (>80%) of transu-dates will have a cell count of less than 1,000/cu mm, while exudates will have a cell count of more than 1,000/cu mm. However, a cell count is of very limited, if any, diagnostic value. Examination of a stained smear and the differential cell count is most useful and may well be diagnostic when ma-lignant cells are identified. Centrifuge 10 ml of fluid, pour out all the supernatant except 0.5 to 1 ml (depending on the thick-ness of the sediment), mix the bottom thoroughly, smear sev-eral slides, and stain with a Wright stain as for a blood smear.

The "normal" cell of the pleural fluid is the lymphocyte, with only some neutrophils present in the fluid. In addition, when the pleura is inflamed, the mesothelial cells that line the normal pleural cavity exfoliate into the effusion. These are large cells with a basophilic cytoplasm and a large nucleus with finely stripped chromatin and one to three blue nucleoli. Most exudates have more than 5% mesothelial cells. A cellu-lar effusion characterized by heavy lymphocytosis (70% to 90%) and the absence of basophilic mesothelial cells (<1%) should be considered tuberculous and only very rarely neo-plastic. The presence of abnormal-appearing immature lym-phocytes favors lymphoma.

Polymorphonuclear leukocytes predominate in acute infec-tions of the pleura, including early tuberculosis. Acute inflam-

38 Thoracentesis

mation of the pleura from other causes (pancreatitis, pulmo-nary emboli) will also increase the number of neutrophils. The presence of toxic granulation and vacuolation will help differ-entiate bacterial infection from neutrophilia caused by inflam-mation. It is very rare to have more than 50% polymorphonu-clear leukocytes in malignant neoplasms.

Eosinophilia (>5% of polymorphonuclear leukocytes) is un-common (1% of pleural effusions). It is almost always in a uni-lateral blood-tinged or hemorrhagic effusion. Its presence, par-ticularly if greater than 10%, speaks against tuberculosis and malignant neoplasms unless a pneumothorax develops. In the majority there is an accompanying peripheral eosinophilia. Closed chest trauma, a viral pleuritis, or a resolving para-pneumonic effusion are its most likely causes.

I. Cytology When a tumor is suspected, at least three separate specimens should be submitted for cytologic examination. The first will be positive for malignant cells in 50% to 60% of ef-fusions caused by a malignant neoplasm. With the three spec-imens the positive yield is increased to 90%, depending on the skill and diligence of the cytopathologist. Degenerating me-sothelial cells may yield false positive results in 2% to 3% of samples examined.

J. Bacteriology Bacteriologic studies on the pleural fluid are extremely important, particularly when an infection is enter-tained as the cause of the effusion. The yield from routine cul-tures is low, but they should probably be done on all diagnos-tic thoracentesis. If the fluid is purulent or has a feculent odor, anaerobic cultures should also be done. Even in known cases of tuberculous effusions, the yield of positive cultures is about 25% to 30%. The possibility of obtaining tubercle bacilli on culture is increased by culturing larger volumes of the fluid (100 ml) or culturing the sediment from a centrifuged sample (100 to 200 ml) of fluid. A Gram stain of the smear, prepared at the same time as the Wright stain, should be carefully ex-amined whenever bacterial infection of the pleural fluid is suspected. Positive smears for acid-fast bacilli on pleural fluid of patients with tuberculous pleurisy are uncommon but should be attempted.

K. Miscellaneous The presence of rheumatoid factor is nonspe-cific. It is high (1:160) in rheumatoid arthritis, but it is also elevated in carcinoma, pneumonia, and tuberculosis. Lupus erythematosus cells are pathognomonic of systemic lupus er-ythematosus and should be carefully searched for when the disease is suspected and the effusion is bilateral. The comple-ment level is low in connective tissue diseases and appears to result from the local consumption of complement. It should be correlated with a simultaneously obtained serum complement

References 29

level. The lowest levels (<15 to 20 units) occur in rheumatoid arthritis and systemic lupus erythematosus and may be de-creased in other diseases (neoplasm, congestive heart failure) but are not as low.

Paired plasma and pleural effusion levels of lysozyme and carcinoembryonic antigen can be useful. Lysozyme concentra-tion is significantly higher in tuberculosis, with a pleural fluid to plasma ratio of over 1.0. The source of lysozyme appears to be the epitheloid cells and activated macrophages. Highest values of lysozyme are in empyemas. Carcinoembryonic anti-gen fluid to plasma ratio of greater than 1.0 will be present in some malignant neoplasms. The pleural fluid carcinoem-bryonic antigen level may be elevated in empyema, tubercu-losis, and mesothelioma. Chromosome analysis combined with fluid cytologic studies will improve the diagnosis of malignant effusions. Abnormalities in the number and structure of chro-mosomes will improve the diagnosis from a single specimen of malignant pleural effusion from 55% to 60% to 80%.

REFERENCES

Lowell J.R.: Pleural Effusion: A Comprehensive Review. Baltimore, University Press, 1977.

An excellent monograph on the subject. Light R.W.: Pleural effusion. Med. Clin. North Am. 61:1339, 1979.

Essential reading for anyone interested in the topic. Stead W.W., Sproul J.M.: Pleural effusion D.M., July 1964, pp. 1 -48 .

A thorough clinical review of pleural effusion. Shank J.C., Latshaw R.F.: Pleural effusion. Am. Fam. Physician 17:143-149, 1978.

A practical, easy-to-read review. Salavid S., Katz S.: Pleural Effusion: Some Infrequently Emphasized Causes. Springfield, 111., Charles C Thomas, Publisher, 1963.

This small book gives a brief literature review, good practical pointers, and illustrative case reports of pleural effusion in pan-creatitis, systemic lupus erythematosus, rheumatoid arthritis, liver cirrhosis, cholesterol, and eosinophilic effusion. Especially well written is the section on eosinophilic pleural effusion.

Black L.F.: The pleural space and pleural fluid. Mayo Clin. Proc. 47:493-506, 1979.

A review of the mechanisms involved in pleural fluid formation and removal, and the effect of disease on these mechanisms.

Chandrasekhar A.J., Buehler J.R.: Diagnostic evaluation of pleural effusion. Geriatrics 29:116-123, 1974.

An easy-to-read, well-written summary of the diagnostic evaluation of pleural effusion.

Leuallen E.G., Carr D.T.: Pleural effusion: A statistical study of 436 Patients. N. Engl. J. Med. 252:79-83, 1955.

30 Thoracentesis

Cause of effusion could not be determined in 25% of patients. In 50% the effusion was neoplastic: of these, carcinoma of the lung accounted for half; carcinoma of the breast, one fourth; and lym-phomas, one eighth. Lymphomas account for half of chylous effu-sions.

Cameron J.L.: Chronic pancreatic ascites and pancreatic pleural ef-fusion. Gastroenterology 74:134-140, 1978.

A superb review. Singer J.A., Kaplan M.M., Katz R.L.: Cirrhotic pleural effusion in the absence of ascites. Gastroenterology 73:575-577, 1977.

Rare but nevertheless true and therefore worth remembering: pleural effusion may develop in absence of detectable ascites. In the presence of small diaphragmatic defects, the negative intrathoracic pressure during inspiration suctions the ascitic fluid into the chest.

Pillay V.K.: Total protein in serous fluids in cardiac failure. S. Afr. Med. J. 39:142-143, 1965.

Rise in protein content (>3 gm/dl) in serous effusion due to cardiac failure occurs following diuresis. This is probably due to the pro-portionately more rapid clearance of water and electrolytes, as the larger protein molecules are not mobilized to the same extent.

Taryle D.A., Potts D.E., Sahn S.A.: The incidence and clinical cor-relates of parapneumonic effusion in pneumococcal pneumonia. Chest 74:170-173, 1978.

When looked for carefully, parapneumonic effusions were present in 57% of pneumococcal pneumonia.

Kirschner P.A., Wisoff B.G.: Use of intravenous catheter for pericar-diocentesis and thoracentesis. J. Mt. Sinai Hosp. 31:433-434, 1964.

Use of an Intracath to drain large amounts of fluid. Kovarik J.L.: Thoracentesis: A modified technique. Postgrad. Med. 48:96-97, 1970.

Describes use of Angiocath to circumvent pneumothorax. Light R.W., MacGregor M.I., Luchsinger P.C., et al.: Pleural effu-sions: The diagnostic separation of transudates and exudates. Ann. Intern. Med. 77:507-513, 1972.

All but one of the exudative fluids studied had at least one of the three criteria (see text), whereas only one transudate had any of the three criteria.

Yam L.T.: Diagnostic significance of lymphocytes in pleural effu-sions. Ann. Intern. Med. 66:972-982, 1967.

In effusions that are predominantly (>50%) lymphocytic, the qual-itative examination of a smear of the sediment is more informative and less time-consuming than the total counts. Beautiful illustra-tions, some in color, of the cells to watch for.

Light R.W., Erozan Y.S., Ball W.C.: Cells in pleural fluid: Their value in differential diagnosis. Arch. Intern. Med. 132:854-860, 1973.

In 31 exudative effusions with lymphocytic predominance, 30 were due to tuberculosis or neoplasms. No tuberculous effusions had more than 1 % mesothelial cells.

References 31

Dines D.E., Pierce R.V., Franzen S.J.: The value of cells in the pleural fluid in the differential diagnosis. Mayo Clin. Proc. 50 :571-572, 1975.

Pleural fluid RBC counts, WBC counts, and differential WBC counts have no specificity in differential diagnosis of effusions. The findings of tumor cells is the only useful finding in differential cell counts.

Bower G.: Eosinophilic pleural effusion: A condition of multiple causes. Am. Rev. Respir. Dis. 95 :746-751 , 1967.

In a significant number of cases, the cause of effusion will remain unexplained. Its presence speaks against tuberculosis.

Curran W.S., Williams A.W.: Eosinophilic pleural effusion: A clue in differential diagnosis. Arch. Intern. Med. 111:809-813, 1963.

Eosinophilic pleural effusion occurs in patients with fungal infec-tion.

Potts D.E., Levin D.C., Sahn S.A.: Pleural fluid pH in parapneu-monic effusions. Chest 70 :328-331 , 1976.

Pleural fluid pH measurements may be useful in deciding on early drainage and thus may prevent loculation of pleural effusions as-sociated with acute bacterial pneumonias. In parapneumonic effu-sions, the pH of the pleural fluid separated empyemas and locu-lated effusion (pH < 7.3) from nonloculated effusion (pH >7.3), which resolved spontaneously.

Nystron J.S., Dyce B., Wada J.B. Jr., et al.: Carcinoembryonic anti-gen titers on effusion fluid. Arch. Intern. Med. 137:875-879, 1977.

Either a high fluid titer (>10 nglml) or one in the range of 5 to 9.9 nglml and a fluid to plasma ratio of greater than 2.0 will differen-tiate a malignant from a benign effusion 90% of the time.

Stanford C.F., Munroe N., Laurence D.J.R.: Concurrent assays of plasma and pleural effusion of carcinoembryonic antigen in the di-agnosis of pleural disease. Lancet 2:53, 1978.

The concentration of carcinoembryonic antigen is increased in car-cinoma of the lung, inflammatory disease (empyema, tuberculo-sis), and mesothelioma.

Klockars M., Petterson T., Riska H., et al.: Pleural fluid lysozyme in human disease. Arch. Intern. Med. 139:73-77, 1979.

Except in empyema, pleural fluid lysozyme content is higher and pleural fluid to plasma ratio greater (>1) in tuberculous pleurisy than other causes of effusion. Lysozyme is derived from active tu-berculous lesions: epitheloid cells and activated macrophages.

Hunder G.G., McDuffie F.C., Huston K.A., et al.: Pleural fluid com-plement, complement conversion and immune complexes in immu-nologic and non-immunologic diseases. J. Lab. Clin. Med. 90 :971-980, 1977.

The reduced levels of pleural fluid complement in rheumatoid ar-thritis and systemic lupus erythematosus are probably secondary to complement conversion by immune complexes formed locally.

Petterson T., Klockars M., Hellstrom P., et al.: T and B lymphocytes m pleural effusions. Chest 73:49-51 , 1978.

32 Thoracentesis

Over 95% of pleural fluid lymphocytes are null cells with no surface receptors of either T or B. In tuberculosis, both percent and abso-lute number of T cells are higher than in blood.

Trapnell D.H., Thurston J.G.B.: Unilateral pulmonary edema after pleural aspiration. Lancet 1:1367-1369, 1970.

Unilateral pulmonary edema may develop in the lung that has been compressed by pleural fluid. The authors recommend that the vol-ume of aspiration be kept to less than 1 L if the underlying lung has been compressed for more than 1 week and below 1.5 L in any circumstance.

Brandstetter R.D., Cohen R.P.: Hypoxemia after thoracentesis: A predictable and treatable condition. JA.M.A. 242:1060-1061, 1979.

Significant hypoxemia, sometimes requiring oxygen therapy, oc-curs at 20 minutes to 2 hours after the procedure and is resolved in 24 hours. The degree of hypoxemia correlates directly with the vol-ume of fluid removed.

Storey D., Dines D.E., Coles D.T.: Pleural effusion: A diagnostic di-lemma. J.A.M.A. 236:2183-2186, 1976.

The central issue of this interesting article is cost-effectiveness, probably carried to an extreme, which leads to the recommendation that only measurement of protein content and cytologic examination be ordered routinely on pleural effusion. An algorithm in ordering other diagnostic tests on the fluid is given.

3

Pleural Biopsy

I. INDICATIONS The primary indication for a pleural biopsy is to establish the cause of an otherwise undiagnosed pleural effusion. Pleural biopsy is not indicated if the effusion is a transudate. Pleural biopsy is not an emergency procedure and it should be done only during routine working hours when adequate support, if needed, is readily available.

With indiscriminate pleural biopsy on all cases of pleural effu-sion, the diagnostic information obtained will be low (12% to 15%); when effusions occurring as part of a known clinical pic-ture (cardiac failure, liver cirrhosis, renal disease, collagen dis-ease, pneumonia, chest trauma, and pulmonary emboli) are ex-cluded, the diagnostic yield is high (60% to 70%).

Consequently, pleural biopsy is not indicated in most pleural effusions but it should be done at the time of initial thoracentesis in cases of pleural effusion of undetermined cause.

II. CONTRAINDICATIONS

A. Uncooperative or confused patient Such a patient might enhance the likelihood of laceration of the lung or subdia-phragmatic viscera.

B. Severe respiratory insufficiency The presence of severe re-spiratory insufficiency, if not due to pleural effusion and therefore likely to improve by thoracentesis, might result in serious consequences should a partial pneumothorax compli-cate the biopsy procedure.

C. Coagulation defect or prothrombin time of less than 50% of control value This should be corrected prior to attempting pleural biopsy.

D. Absence of pleural fluid This is not a true contraindication, since in experienced hands biopsy done in the absence of fluid can be diagnostically as successful as that done in the pres-ence of fluid. However, because of the greater incidence of complications with biopsies performed in the absence of fluid, the procedure should be reserved for a skilled specialist.

33

34 Pleural Biopsy

E. Empyema

III. TECHNIQUE The usual needles used for pleural biopsy are ei-ther the Cope or the Abrams needle. The Cope needle consists of different parts and is the needle generally used for pleural biopsy

Aspiration trocar

O u t e r - c a n n u l a

Hooked biopsy trocar i-

Fig 3-1.—Components of Cope biopsy needle and technique for obtaining pleural tissue. With aspiration trocar inside the outer can-nula a, insert needle to just inside pleural space or effusion; b, re-move aspiration trocar; c, insert hooked biopsy trocar; d, withdraw outer cannula to just outside pleural space; e, with outer cannula held stationary, slowly withdraw biopsy trocar to engage pleura in hooked tip of biopsy trocar (resistance will be felt, indicating that pleura has been hooked); f, transect hooked specimen by rotating cannula back and forth between thumb and index fingers holding it. Remove biopsy trocar, leaving outer cannula in place. Extract spec-imen. Repeat procedure with hooked biopsy trocar, obtaining addi-tional specimens from four quadrants around point of entry.

Technique 35

(Fig 3 -1 ) . Always check the needles to be sure that they are com-patible with the trocar and that they slide in and out of the trocar easily before you begin the procedure. By roentgenogram and chest percussion, determine the location of the pleural effusion as for a thoracentesis.

A. Assemble proper equipment The tools are the same as those used for thoracentesis, with the addition of a Cope biopsy nee-dle (see chapter 2).

B. Prepare patient as for thoracentesis Note the depth of the needle when fluid is obtained during the instillation of anes-thetic. Remember to always aspirate as the needle is ad-vanced. Using the tip of a No. 11 blade, make a small nip in the skin at the point of entry.

C. Obtain pleural fluid Assemble 10- to 30-ml syringe, pointed trocar, and outer cannula (with cutting edge). Advance this above the rib. Remember that the intercostal artery, vein, and nerve run their course below the ribs (see Fig 2 - 1 ) . Advance while aspirating until pleural fluid is obtained. Withdraw can-nula while aspirating until no fluid is obtained, such that the tip of the cannula is just outside the pleural space.

D. Aspirate fluid Have the patient exhale, thus increasing his intrapleural pressure; simultaneously remove the inner trocar and immediately cover the end of the cannula (see Fig 3 -1 ) . Insert the blunt-tipped biopsy trocar connected to a 10-ml sy-ringe into the cannula. Note that the long lip of the hilt of the biopsy trocar points in the same direction as the hook. To avoid contaminating the pleural fluid with blood, you may now aspirate enough fluid for diagnostic purposes.

E. Perform biopsy Point the lip (and thus the hook) down to-ward the rib. Withdraw both the cannula and biopsy hook to-gether, applying pressure in the direction of the lip until the instrument is felt to catch the parietal pleura (see Fig 3 -1) . While holding the hilt of the biopsy hook, push the cutting outer cannula with a rotating motion back into the pleural space. This motion cuts off the piece of pleura caught in the hook and restores the cutting cannula to a position inside the pleural cavity. Withdraw the biopsy hook as the patient ex-hales, again covering the end of the cannula after withdrawal of the biopsy trocar.

F. Remove the tissue obtained and place it in a fixative bottle.

G. Repeat procedure Reinsert the biopsy trocar, and repeat the procedure. Two more specimens of tissue should be obtained. Turn the hook so that the pieces are obtained from each of the lateral quadrants of the point of insertion. In this manner, the so-called three-quadrant tap is obtained. Never obtain a bi-

36 Pleural Biopsy

opsy specimen from the upper or fourth quadrant as the ma-terial may contain nerve and arterial wall and biopsy of this quadrant may have most undesirable consequences.

H. Aspirate remainder of pleural fluid When the necessary tis-sue is obtained, the remainder of the pleural fluid may be as-pirated through the cannula.

I. Remove entire assembly and apply pressure to biopsy site.

IV. COMPLICATIONS Pleural biopsy by the technique described is a simple, safe, convenient, and productive diagnostic procedure. In about 1,000 cases compiled from the literature, the complica-tion rate was about 5% and the morbidity rate was approxi-mately 0.3%.

A. Pneumothorax Obtain a postbiopsy chest roentgenogram on all patients to determine whether a pneumothorax has oc-curred. Small pneumothoraces of about 5% to 15% of lung vol-ume occur in 2% to 5% of patients. These are usually asymp-tomatic, respond to conservative treatment, and generally will absorb spontaneously in a few days. Pneumothoraces of over 25% require immediate surgical consultation for possible tube thoracostomy.

B. Hemorrhage If the cutting needle is inadvertently directed upward and the intercostal artery is lacerated, profuse bleed-ing may occur. Should this be documented by dropping hema-tocrit readings, deteriorating respiratory function, or hemor-rhagic thoracentesis fluid, consult a thoracic surgeon immedi-ately.

Occasionally, a subcutaneous hematoma develops at the bi-opsy site.

C. Infection Subcutaneous abscess may develop at the biopsy site in patients with empyema. A tuberculous nodule has also been reported to develop at the biopsy site in a patient with tuberculosis.

D. Visceral biopsy Inadvertent lung tissue or, more rarely, liver tissue may be obtained, particularly when the pleural biopsy is attempted in the absence of an effusion.

E. Carcinomatous implantation along the needle tract This rare complication does not affect the prognosis of patients with malignant pleural effusions. The lesion responds to local ra-diotherapy.

V. INTERPRETATION Pleural biopsy is primarily helpful in differ-entiating tuberculous from neoplastic effusions. As in any closed-needle aspiration procedure, positive results will depend on the

Interpretation 37

diffuseness of the disease process, so that the rather tiny (2 x 3-mm) biopsy specimen is representative of the specific pathologic process. When the process is diffuse, as in tuberculosis, the biopsy specimen will be diagnostic in the majority of cases (70% to 80%). However, when pleural involvement is spotty, as in metastatic lesions, the biopsy tissue may be obtained from between the is-lands of abnormality and therefore may not be representative of the underlying disease.

A granulomatous reaction in a pleural biopsy specimen is vir-tually always due to tuberculosis. Histoplasmosis and sarcoidosis, the other two common granulomatous diseases of the lung, only rarely cause pleural effusions. However, even caseating granulo-matous reactions are compatible with, rather than diagnostic of, tuberculosis. Culture of tubercle bacilli provides the most secure evidence that the disease process in question is tuberculosis. The rate of positive culture of the pleural biopsy specimen is greater (55% to 75%) than that of multiple pleural fluid cultures (about 30%). A piece of tissue should, therefore, always be cultured when tuberculosis is suspected. A liquid medium (Dubos) is su-perior to a solid medium (Lowenstein-Jensen). Grinding the spec-imen prior to inoculation has been reported by some authors to be more successful; other authors disagree, because of bacterial contamination at the time of maceration. The specimen can be sent to the laboratory in sterile saline. Prior antituberculous therapy should not preclude an attempt to culture tubercle ba-cilli. When culture results of a biopsy specimen and its histologic findings are combined, the overlap will give a diagnosis in up to 95% of cases of tuberculosis. Thus there is a definite enhance-ment of the diagnostic value of a pleural biopsy by culturing a fragment of tissue.

Positive smears for acid-fast bacilli are rare on biopsy speci-mens. False positive results occur and have on occasion been traced to saprophytic contamination of the water supply used in preparation of the stains. Nevertheless, special stains, including silver methionine for fungus and carbol fuchsin for tuberculosis, should be done.

In 40% to 60% of patients with neoplasia, a definite diagnosis can be made from the biopsy specimen. The yield is higher for carcinoma of the lung than for lymphomas. This is not only be-cause of the spotty nature of the lesion but also because in malig-nant neoplasms (particularly lymphomas) the effusion may be due to lymphatic obstruction rather than to pleural seeding. Un-like tuberculosis, where the yield of effusion culture is low, in cases of neoplasm the yield of cell block (40% to 60%) approxi-mates the yield of biopsy and is often positive when the biopsy specimen is negative (20%). When the results of biopsy and fluid cytologic study are combined, a positive diagnosis will be made in 85% of cases of neoplastic pleural effusion.

In about one third of cases, a histologic diagnosis cannot be

38 Pleural Biopsy

established and the tissue is reported to reveal nonspecific in-flammatory reaction. This cannot be used to exclude either tuber-culosis or neoplasms and should evoke additional diagnostic ef-forts since a third of these will be tuberculous or neoplastic in origin. Other causes of nonspecific inflammation are unsuspected pulmonary infarction, pneumonia, empyema, and bronchiectasis.

Some 20% of specimens will be normal pleura or will in some respect be insufficient for diagnosis. A second biopsy in these cases, as well as in those with specimens interpreted as nonspe-cific inflammatory reaction, will yield a diagnosis in about 30%. A third biopsy will yield a diagnosis in about 10% to 15%.

No pleural tissue may be obtained in 4% to 10% of cases. In-ability to obtain tissue depends on the skill and experience of the operator, the amount of free fluid present, and the thickness of the parietal pleura. Failure to obtain tissue at the time of the initial biopsy may be reduced by repeating the procedure through the same incision with the biopsy needle directed in at least three different directions, except, of course, superiorly, to avoid lacera-tion of the subcostal vessels.

To the extent that the biopsy can be helpful only where specific changes can be demonstrated, failure to obtain tissue or a diag-nosis on the tissue obtained should suggest consideration of an open pleural biopsy.

REFERENCES

DeFrancis N., Kiosk E., Albano E.: Needle biopsy of the parietal pleura. N. Engl. J. Med. 252:948-949, 1955.

The Vim-Silverman needle technique. Abrams L.D.: A pleural-biopsy punch. Lancet 1:30-31, 1958.

The Abrams needle is described by the author, who designed and introduced it at Harefield Hospital; hence the two names of the nee-dle: Abrams or Harefield.

Cope C.: New pleural biopsy needle. J.A.MA. 167:1107-1108, 1958. The Cope needle technique.

Cope C., Bernhardt H.: Hook-needle biopsy of pleura, pericardium, peritoneum and synovium. Am. J. Med. 35:189-195, 1963.

The many applications of the Cope needle biopsy and its technique. Schools G.: Needle biopsy of parietal pleura: Current status. Tex. Med. 59:1056-1061, 1963.

A good comparative summary of the various pleural needle biopsy methods.

Niden A.H., Burrows B., Kasik J.E., et al.: Percutaneous pleural bi-opsy with a curetting needle: Special reference to biopsy without ef-fusion. Am. Rev. Respir. Dis. 84:37-41, 1961.

An adequate specimen of tissue was obtained in 17 patients who had biopsies in the absence of pleural fluid. In three patients an asymptomatic pneumothorax developed after biopsy.

Mestitz P., Purves M.J., Pollard A.C.: Pleural biopsy in the diagnosis

References 39

0f pleural effusion: A report of 200 cases. Lancet 2 :1349-1353 , 1958. The biopsy specimen established a diagnosis in 104 cases (71 tuber-culosis and 33 neoplasm), was not diagnostic in 92 cases, and was inadequate in 4.

Donohoe R.F., Katz S., Matthews M.J.: Pleural biopsy as an aid in the etiologic diagnosis of pleural effusion: Review of the literature and report of 132 biopsies. Ann. Intern. Med. 48 :344-362 , 1958.

Histologic diagnosis was established by biopsy in 73% of cases of tuberculous pleurisy and in 50% of cases of neoplastic effusions. Both tuberculosis and cancer may be present, yet the pleural biopsy specimen will demonstrate only nonspecific changes.

Hampson F., Karlish A.J.: Needle biopsy of the pleura in the diag-nosis of pleural effusion. Q. J. Med. 30:249-255, 1961.

In cases of tuberculosis, biopsy was diagnostic in 75%, but when all methods of investigation (culture) were included a definite di-agnosis was possible in 94%. In cases of cancer, biopsy was diagnostic in 62.5%, but when all methods were included (cytologic study, bronchoscopy) correct di-agnosis was attained in 85%. In 65 biopsy specimens interpreted as nonspecific, the final diag-nosis was as follows: tuberculosis, 5; malignancy, 14; empyema, 13; rheumatoid arthritis, 3; pneumonia, 12; congestive heart fail-ure, 4; pulmonary infarction, 7; and miscellaneous, 7.

Sison B.S., Weiss W.: Needle biopsy of the parietal pleura in patients with pleural effusion. Br. Med. J. 2 :298-300 , 1962.

In a series of 185 consecutive patients, pleural biopsy by house of-ficers in a general hospital revealed tuberculosis in 28%, malig-nancy in 12%, nonspecific fibrosis in 25%, normal pleura in 15%, and inadequate tissue in 20%. The biopsy gave a yield of specific findings in 61 % of patients with tuberculosis and 59% of patients with neoplastic effusions.

Levine H., Agell D.W.: Blunt-end needle biopsy of pleura and rib. Arch. Intern. Med. 109:516-525 , 1962.

A specific diagnosis on the basis of biopsy was achieved in 83% of patients with tuberculous effusion and 75% of those with neoplastic effusion. Not all specific diagnostic biopsy specimens were achieved with the first attempt. Of 70 diagnostic biopsy specimens, 57 were positive on the first attempt, 7 on the second, and 6 on the third or fourth attempt.

Rao N.V., Jones P.O., Greenberg S.D., et al.: Needle biopsy of pari-etal pleura in 124 cases. Arch. Intern. Med. 115:34-41 , 1965.

A histologic diagnosis was established in two thirds of the cases. Scerbo J., Keltz H., Stone D.J.: A prospective study of closed pleural biopsies. JA.MA. 218 :377-380 , 1971.

Biopsies done in the absence of pleural fluid were as diagnostically successful as those done in the presence of fluid. Repeat biopsy in-creased diagnostic yield: 29% were positive with the initial biopsy, 28% with the second attempt, and 11% with the third attempt. In

40 Pleural Biopsy

biopsy specimens interpreted as showing nonspecific pleural reac-tion, the eventual diagnosis was neoplasm in 40%, tuberculosis in 19%, and pulmonary infarction in 16%.

Berger H.W., Mejia E.: Tuberculous pleurisy. Chest 63:88-92, 1973. A critical, concise, but complete review of the topic.

Weiss W.: Needle biopsy of the parietal pleura in tuberculosis. Am. Rev. Respir. Dis. 78:17-20, 1958.

Caseating tubercles were seen in 23 of 31 cases with effusion; cul-ture of the pleural fluid was positive for tubercle bacilli in 16 of 27; and the diagnosis of tuberculosis was established in 27 of 31, whereas it remained idiopathic in 4.

Wichelhausen R.H., McLean R.L., Lowery F.B.: Reinforcement of di-agnostic value of pleural biopsies by culture in liquid medium. Am. Rev. Respir. Dis. 93:288-290, 1956.

A punch biopsy specimen of pleura is a suitable specimen for bac-teriologic studies, with approximately a 40% positive yield for tu-bercle bacilli. The search for the organism on stained specimens is less rewarding, with about 15% positive.

Scharer L., McClement J.H.: Isolation of tubercle bacilli from needle biopsy specimens of parietal pleuras. Am. Rev. Respir. Dis. 97:466-468, 1968.

Tubercle bacilli were cultured from 55% of biopsy specimens, in contrast to 23% from pleural fluid. Histologic study was diagnostic in 63% of cases; histologic plus bacteriologic study increased the diagnostic yield to 80%.

Levine H., Metzger W., Lacera D., et al.: Diagnosis of tuberculous pleurisy by culture of pleural biopsy specimen. Arch. Intern. Med. 126:269-271, 1970.

In proved cases of tuberculosis, histologic study was positive in 71.4%; tubercle bacilli grew from culture of the biopsy specimen in 76.2%. When culture results of biopsy and histologic study were combined, the overlap resulted in a correct diagnosis in 95%. Cultures of the pleural biopsy specimen were positive with greater frequency (76.4%) than multiple cultures of the pleural fluid (47.6%) or of sputum and gastric lavage specimens (33.3%).

Samuels M.L., Old J.W., Howe C.D.: Needle biopsy of the pleura: An evaluation in patients with pleural effusion of neoplastic origin. Cancer 11:980-983, 1958.

Best results were found on biopsy specimens obtained in broncho-genic carcinoma (57%) and poorest results with malignant lym-phoma (36%). Needle biopsy complements pleural fluid cytologic study: 8 cases had a positive biopsy specimen but negative cytologic study, whereas 6 had a negative biopsy specimen but positive cytologic study.

Schachter E.N., Basta W.: Subcutaneous metastasis of an adenocar-cinoma following a percutaneous pleural biopsy. Am. Rev. Respir. Dis. 107:283-285, 1973.

A rare complication that does not affect the prognosis of patients

References 41

with malignant effusions and should not serve as a contraindica-tion to pleural biopsy.

f-lamel N.C., Briggs J.N., Ludington L.G.: Cancer of the lung in the tuberculosis patient. Calif. Med. 91:131-133, 1959.

Cancer of the lung occurs in tuberculous patients. Of all tubercular patients admitted over 45 years, 1.4% also had cancer of the lung.

15

Abdominal Paracentesis

I. INDICATIONS

A. Diagnostic While it may not be necessary to perform para-centesis routinely in patients with chronic ascites with an ob-vious underlying cause for the ascites (cirrhosis, nephrotic syndrome, congestive heart failure, or other rare causes of as-cites not associated with peritoneal disease), no patient with ascites can be considered to have been completely evaluated without this examination. In 10% or more of the larger series of ascites evaluation, more than one pathologic finding is pres-ent, mostly in association with cirrhosis of the liver. Specifi-cally, because of their occurrence in the heavy alcohol con-sumer, a number of peritoneal diseases manifesting with as-cites (pancreatitis, tuberculosis, malignant neoplasms, spon-taneous bacterial peritonitis) may be mistaken for cirrhosis. Certainly, in the patient with chronic ascites with fever, ab-dominal pain, diarrhea, or acute deterioration there should be no question about the necessity of a diagnostic paracentesis.

In patients with acute ascites, a diagnostic paracentesis should be performed even if the cause of ascites seems obvious, unless a serious contraindication is present.

In the evaluation of blunt trauma to the abdomen, an ab-dominal tap, possibly with peritoneal lavage, can prove inval-uable in determining the need for surgical intervention. In the unresponsive comatose patient with possible abdominal inju-ries, an abdominal tap to determine intra-abdominal involve-ment can prove lifesaving.

B. Therapeutic Therapeutic abdominal paracentesis may be performed for (1) relief of abdominal pain and discomfort of a taut abdomen, (2) relief of dyspnea or orthopnea caused by an elevated diaphragm and its consequent diminished respiratory capacity and undesirable pulmonary basal segment hypoven-tilation and atelectasis, (3) reduction of intra-abdominal pres-sure in which a tense abdomen may be detrimental, as in an incarcerated hernia or variceal hemorrhage, (41 institution of

42

Contraindications 43

peritoneal dialysis in the patient with renal failure or ascites reinfusion in the cirrhotic patient with ascites not controlled by diuretics and salt restriction, or (5) recurrent severe and symptomatic distention of malignant ascites not readily con-trolled by salt and water restriction or diuretics.

When ascites is removed for therapeutic purposes, it must be remembered that the rapid removal of large volumes can result in shock and deterioration of renal function. As a rule, in the patient with abnormal liver function, removal should be limited to a maximum of 1 L, which is sufficient to accom-plish the desired cardiopulmonary improvement while circum-venting the complications associated with removal of large volumes.

II. CONTRAINDICATIONS All of the following constitute relative contraindications to paracentesis. Paracentesis in these condi-tions is associated with a certain risk, and the procedure should be either postponed until the condition is corrected or confined to those situations where it will provide essential information.

A. Bowel distention Intraperitoneal soiling secondary to bowel laceration and puncture is more likely to occur when the in-testinal loops are either distended or abnormal secondary to ileus or obstruction. An attempt should be made to decompress the bowel by intubation prior to paracentesis.

B. Bleeding disorder Evaluate patients with prothrombin time, partial thromboplastin time, and some measure of platelet function (bleeding time, platelet count, or adequacy on smear) prior to performing paracentesis. These are particularly im-portant in the patient with organomegaly or distended bowel loops. If the test results are only modestly disturbed, careful paracentesis strictly restricted to the vascular midline below the umbilicus, using a small-gauge needle and after infusion of fresh frozen plasma, may be done without added risk. In the patient with severe bleeding diathesis, the risk of bleeding outweighs the benefits of paracentesis and the procedure should be postponed until the bleeding disorder is corrected.

C. Multiple abdominal scars The loops of bowel generally slip away from the point of the needle, unless they are adherent to the parietal peritoneum at the puncture site, in which case the risk of perforation or laceration is increased. Areas of pre-vious surgical scars should therefore be avoided, but when there are multiple scars the risk is magnified, as adhesions may be present even in areas under normal skin.

D. Local infection Avoid areas of diseased skin. Skin infections near puncture sites may result in contamination of the peri-toneal space or poor healing of the puncture site.

44 Abdominal Paracentesis

III. TECHNIQUE

A. Assemble proper equipment The paracentesis tray should include antiseptic for skin preparation, sterile drapes, cotton balls, gauze squares, sponge forceps, sterile gloves, anesthetic solution, 10-ml syringe, 22-gauge 3.75-cm needle, sterile test tubes, a plastic catheter-needle combination (Intracath), and a peritoneal dialysis catheter set or an 18-gauge spinal tap needle.

B. Examine abdomen Ascertain the presence or absence of hep-atosplenomegaly, renal or ovarian cysts, a gravid uterus, aor-tic aneurysms, visible collateral venous channels, or massive bowel dilatation.

C. Select puncture site The lower quadrants, at least 1 cm lat-eral to the vertical borders of the rectus muscle, or the rela-tively avascular midline, midway between the umbilicus and the upper pubic ridge, are preferred (Fig 4 - 1 ) . Surgical scars must be avoided. The rectus muscles contain the network of superficial and inferior epigastric vessels and must be avoided. The anatomy of the rectus muscle can be easily outlined by having the patient try to sit up from the lying position with-out leaning on his arms (brace arms on chest or clasp hands behind the head). Taps in the upper quadrant are best avoided and should be done only after ascertaining the liver and spleen borders in order to avoid inadvertent visceral puncture.1

D. Have bladder emptied Ask the patient to void. Percuss the bladder to ascertain that it is empty. If any doubt exists, cath-eterize the bladder. This is particularly important in the el-derly or comatose patient; otherwise, voluntary voiding should suffice to decompress the bladder.

E. Position patient The supine position is preferred. Alterna-tively, the semisitting Fowler position in bed or upright sit-ting on the side of the bed with the feet on a chair or stool may be used.

F. Clean abdomen Using sterile technique (masked and gloved), cleanse and drape the entire abdomen. If a four-quad-rant tap is contemplated, draping may be omitted.

G. Anesthetize puncture site Using a small needle, infiltrate the skin in the midline about 2 cm below the umbilicus or the alternate sites in the lower or upper quadrants (see Fig 4 - 1 ) . Change to a larger needle, and infiltrate the anesthetic solu-tion through the abdominal wall.

H. Introduce needle into peritoneal cavity A small-caliber nee-dle is preferred. The use of a spinal needle or an Intracath does not require preliminary skin incision, whereas the use of

Technique 45

Li rxe<s , S i l b a ^

Lai. margin of rectus sheam

_ ' o i n t s o f e r v t r y

E p i ^ a i n x c a c r t e : r y

Fig 4-1.—Points of needle entry for abdominal paracentesis. Lower quadrants or relatively avascular linea alba, at a point 2.5 to 5 cm below umbilicus, are preferred. Upper quadrants are best avoided because of risk of undetected hepatosplenomegaly in patient with ascites. Rectus muscle must be avoided because of risk of pierc-ing epigastric blood vessels.

a trocar or a peritoneal dialysis catheter, because of their larger size, require skin incision and are more likely to result in leakage afterward.

Insert the needle attached to a syringe and advance it per-pendicular to the skin, with a rotating motion and gentle pres-sure, until its point is thought to be several millimeters within the peritoneal cavity. A "snap" or "give" usually can

56 Abdominal Paracentesis

be felt as the needle passes the thick anterior muscular fascia, and another as it passes the thick posterior muscular fascia. Occasionally, the peritoneal layer can be felt as a separate, less pronounced snap. The sudden release of resistance once the peritoneum is pierced should be anticipated (from the dis-tinct increase in resistance felt as the needle reaches the peri-toneum) to avoid an unexpected forward thrust of the needle. At this point the needle may be held fixed with gentle pres-sure and the patient asked to cough and tense the abdominal wall against it until the "pop" of the peritoneum is felt.

If a combination needle-catheter or peritoneal dialysis set is being used, introduce the catheter into the abdominal wall while the needle is held firmly in place.

I. Collect fluid Fluid is collected either by a syringe or by let-ting the fluid run into a collecting tube.

J. Process fluid samples Depending on the purposes of the tap, collect fluid in the appropriate containers for any and all of the following determinations: specific gravity, protein, LDH, glucose, cell count and differential cell count, culture (bacte-rial and acid-fast bacilli), Gram stain (by physician), exfolia-tive cytologic study (60% alcohol solution), amylase, and tri-glycerides. A simultaneous blood sample for glucose, protein, amylase, and LDH determinations should be obtained.

K. If fluid is not obtained Advance needle slowly with gentle suction if fluid is not obtained. The needle may be rotated or angulated in search of free fluid. These maneuvers must be performed with the needle point just inside the peritoneum. The needle should move only along its axis, either forward or backward, to avoid intraperitoneal lacerations. To reposition the needle, pull it back to the peritoneum, point it in the di-rection selected, and advance it. If these maneuvers fail to yield fluid, remove the needle while applying gentle suction. Other areas may be tried with the same process.

If no fluid appears in any location, withdraw the needle from the abdomen and push air through it while it is held close to a glass slide. A stained preparation of minute amounts of fluid obtained by this "squirt" technique may provide help-ful diagnostic clues.

L. In cases of acute abdominal injury Lavage peritoneal cavity with 1 L of warmed normal saline in cases of acute abdominal surgery. This may increase the diagnostic accuracy of deter-mining intra-abdominal or visceral injury or hemoperitoneum. The saline should be run in rapidly and allowed a dwell time of 10 minutes, during which the patient should be encouraged or assisted to move around, and then it should be drained.

M. There is a positive correlation between the amount of fluid present in the abdominal cavity and a positive tap. At vol-

Complications 47

umes exceeding 350 ml, the yield is 70% to 80% and justifies the procedure. At volumes exceeding 500 ml, the chance of obtaining fluid is increased to 85% to 90%. A negative tap greatly reduces the likelihood that substantial fluid is present.

N. Removal Of fluid As a rule, no more than 1 L of fluid should be removed at a time, especially if the fluid is a transudate, because of the risk of compromising the effective circulating blood volume. With exudative effusions, especially secondary to malignancy, larger volumes may be removed with less risk. Studies have shown that the maximum therapeutic benefit of dyspnea, pain, oliguria, etc., is achieved with removal of only 1 L of ascitic fluid.

IV. COMPLICATIONS Paracentesis is a relatively simple and safe procedure. If the proper technique is followed and sensible pre-cautions are taken, the complication rate is less than 1%. The risks are increased somewhat (2% to 3%) in patients with alco-holic liver disease.

A. Hemorrhage Depending on the site of the traumatized ves-sel, hemorrhage may occur into the abdominal wall (epigastric vessels) or into the peritoneal cavity (omental varices, neo-plastic implants). Localized abdominal wall bleeding can be controlled by pressure. Intraperitoneal bleeding is more diffi-cult to control and, if massive, may result in shock and prove fatal unless it is detected early and corrected surgically. Major bleeding is more common and severe in taps of neoplastic as-cites, while minor bleeding is more frequent in patients with cirrhotic ascites with undetected clotting abnormalities.

B. Bowel perforation The needle rarely perforates the bowels, which generally slip away from it, except in the presence of adhesions, which bind and fix the intestinal loops to the ab-dominal wall at the puncture site. Avoiding areas of previous surgical incisions should circumvent this complication.

In experimental studies, penetration of the abdominal wall with large numbers of needles of varying size and gauge has shown a low incidence of perforations. Even after purposeful bowel puncture in as many as 250 different points along the gastrointestinal tract, no peritonitis results. Intraluminal pressures of 260 to 280 mm Hg for the small intestine and 350 mm Hg for the colon are required to cause leakage through perforations made with a 20-gauge needle in the dog. In man, the highest pressures developed with total obstruction are 200 to 300 mm H 2 0 in the small intestine and 300 to 500 mm H 2 0 in the colon. Thus, while laceration or puncture of the bowel during paracentesis may occur (even if more commonly than appreciated), the self-sealing action of the gut wall and the natural defenses of the peritoneum usually prevent leakage

48 Abdominal Paracentesis

T a b l e 4 - 1 A S C I T I C F L U I D CHARACTERISTICS*

TOTAL WBCs GROSS SPECIFIC PROTEIN CU

TYPE APPEARANCE GRAVITY (Gm/Dl) MM

Cirrhotic Clear 1,006-1,020 <2.5 <300 (90%<1,015) (Up to 4 (90%<500)

in 15%) (20-2,000) Neoplastic Clear 60% 1,008-1,020 >2.5 <1,000

Bloody 25% (95%<4.5) (300-1,000) Chylous 15% (2-5)

Cardiac Clear 1,008-1,020 <3.5 <300 (2-5)

Pancreatic Clear 60% Sanguineous 1,008-1,025 >3 in 76% 300-1,000

30% Turbid 7% <2 in 10% Chylous 3% (3-6)

Nephrotic Clear 1,006-1,014 <1.0 <300 Tuberculous Clear

Cloudy (rare) 1,008-1,026 >2.5 >500 (3.5-7.5) (150-2,800)

Spontaneous Cloudy 1,009-1,025 <2.5 >500 bacterial (500-20,000) peritonitis Usually >1,000

Myxedema Viscous 1,010-1,020 >3.5 <200 Chronic >1,015

renal disease Clear (1,015-1,025) >4 >300 (dialysis) (1.5-6.5) (30-1,500)

Starch Cloudy >1,015 >3.5 >4,000 peritonitis Amber (1,010-1,020)

*Values are means, with ranges given in parentheses; N, normal; LDH,

and peritonitis. When peritonitis does occur it will be a mixed bacterial peritonitis with two to three causative organisms.

This rather reassuring information notwithstanding, it is always alarming to observe the appearance of air or fecal con-tents in the paracentesis syringe. In all such cases, remove the needle in the same line as it was introduced and observe the patient closely for the ensuing 24 hours. The majority of punc-tures will seal and heal without the need for surgical inter-vention.

C. Persistent leakage of ascitic fluid is more likely to occur in the presence of massive and tense ascites, particularly when large-gauge needles are used. In the presence of a traumatic fistula, induced at the time of paracentesis, this will dissect downward into the abdominal wall and result in abdominal

Complications 49

POLYMOR-PHONUCLEAR LYMPHOCYTES

LEUKOCYTES (%) (<*) GLUCOSE COMMENTS

<25 (2-98)

<45

<25

85 ( 2 - 1 0 0 )

75

90

N

Decreased

N

Cytologic studies positive in 60%-80%

25-75 25-75 N Elevated amylase level in 99%

<25

<20

>75

<20

<15

<35

lactic dehydrogenase.

85

>80 (75-96)

<25

>80

>85

>65

N

Decreased

Decreased

N

N

N

Culture positive in 50%-80%

Biopsy positive in 90% Smear positive in <5% Culture positive in 99% Smear positive in <5%

Elevated LDH level

Positive iodine stain Maltese crosses by

polarized light microscopy

wall, scrotal, penile, or labial edema. In the event of an exter-nal leak, sutures are best avoided as they result in the for-mation of new connections for the ascitic fluid to dissect into the abdominal wall as well as creating a nidus for infections. Leaks are best controlled with absorbent dressing and will stop in a few days. If this fails, try to suture.

D. Postparacentesis shock and hyponatremia If excessive vol-umes (> 1 L) of fluid are removed in patients with cirrhotic ascites, particularly if the patients are hypoalbuminemic, shock, oliguria, and hyponatremia will occur. In such cases, replace volume with isotonic fluid without concern for the reaccumulation of ascites.

E. Abdominal wall abscess Observe the whole area around the

162 Arterial Line Placement

Prospective study of the risk of thrombosis and infection. N. Engl J Med. 290:1227-1231, 1974. ' '

In a prospective study of over 500 patients, hypotension, the use of vasoconstrictive agents, and prolonged (1 week) catheterizations were associated with complete arterial occlusion in 3 study patients Partial occlusions, detected by Doppler technique, occurred in 19.3%. No local or systemic infections could be definitely related to catheterization, but catheter-tip culture was positive in 4%.

Bedford R.F., Wollman H.: Complications of percutaneous radial-ar-tery cannulation: An objective prospective study in man. Anesthe-siology 38:228-236, 1973.

Complications encountered following prolonged percutaneous can-nulation were recorded by daily examination and Doppler flow measurements.

15 Central Venous Line

Placement

I. INDICATIONS

A. Central venous pressure measurement While clinically useful, the peripheral venous pressure measured by simple manometry and the jugular venous pressure measured by in-spection are fraught with error and in the critically ill patient are replaced by measurements of the central venous pressure (CVP). The introduction of subclavian venipuncture to place a central venous line did much to popularize measurements of the CVP as an index of the circulating blood volume relative to the pump capacity of the heart. When cardiovascular func-tion is stable, the CVP will vary directly with alterations in blood volume and can be used as an aid in determining the adequacy of fluid replacement in critically ill patients. When blood volume and vascular dynamics are stable, the CVP is expected to vary indirectly with alterations in cardiac pump activity. However, it is incorrect to assume that the right atrial pressure, measured by a properly placed central venous line, correctly reflects on left side heart function, which is bet-ter defined by measurements of left atrial and pulmonary cap-illary wedge pressures (to be covered in chapter 16); hence the greatest limitation of the CVP, which nevertheless remains an indispensable clinical tool.

B. Fluid administration The central venous line should never replace conventional methods of peripheral vein infusions. It should be reserved for the following special situations:

1. Rapid administration of large volumes of fluid or blood in the presence of peripheral vascular collapse.

2. Administration of hypertonic fluids for parenteral hyper-alimentation.

3. Absence of other routes to administer necessary intrave-nous fluids or medications, as in the burned, obese, or to-tal-body-cast patient.

1 6 3

164 Central Venous Line Placement

C. Intracardiac drug administration In emergency situations the central venous line is useful for the rapid delivery of carl diac drugs and vasopressors.

D. Central blood sampling and phlebotomy

E. Atrial electrographs Obviously, the catheter will have to be advanced to the right atrium for this purpose and a stylet electrode passed through it.

F. Insertion of pacing electrodes

G. Right-sided cardiac catheterization and Swan-Ganz catheter placement

H. Pulmonary angiography If a pulmonary embolus is sus-pected, the central venous line can be used to inject contrast material.

II. CONTRAINDICATIONS

A. Availability of a more accessible route

B. Infected skin or burns over area

C. Inexperienced operator This is particularly true of subcla-vian venipuncture, in which the success and complication rate depend on the skill and experience (>50 venipunctures) of the operator. Supervision by an individual with experience is a must to all elective (>95%) subclavian venipunctures.

D. Restless or uncooperative patient

E. Bleeding tendency with abnormal coagulation studies: pro-thrombin time over 15 seconds; platelet count less than 50,000/cu mm.

F. Any of the following chest problems constitutes a contrain-dication to subclavian venipuncture:

1. Any severe or crippling pulmonary disease.

2. Chest deformity.

3. Puncture on the side opposite to that of recent chest trauma, surgery, or chest tube placement.

4. Puncture on the side opposite to that of recent unsuccess-ful subclavian venipuncture attempt without an interim chest roentgenogram.

III. TECHNIQUE Central venous line may be placed by catheteriza-tion of the basilic, subclavian, or internal jugular vein (Fig 15-1). The technique of each of these routes of entry will be de-scribed individually:

Technique 165

Fig 15-1.—Points of entry for basilic, subclavian, and internal jugular vein cannulation.

BASILIC VEIN CATHETERIZATION

The basilic vein, just above the elbow, may be cannulated by percutaneous venipuncture or through a venous cutdown. When-ever possible, a percutaneous venipuncture should be done to avoid the likelihood of sacrificing the vein forever, as is usually the case with a cutdown.

A. Equipment Assemble the necessary equipment prior to un-dertaking the procedure. The equipment should include the following:

1. Tourniquet

2. Cutdown set, including sterile drapes and gloves

3. Cleansing solution, 1% to 29c iodine

4. 1 9c Lidocaine solution

166 Central Venous Line Placement

5. 10-ml syringes, 25-gauge needle

6. Intravenous catheter. Bardic 1 catheter, Abbott-drum-car. tridge catheter (preferred), or 6- or 8-gauge sterile pediak ric feeding tube

7. 3-0 silk suture, thread, needle

8. Adhesive tape

9. CVP manometer

10. Sterile saline, 25 ml

11. Broad-spectrum antibiotic ointment

12. Intravenous fluid bottle, tubing, and stand

B. Venipuncture procedure

1. Position the arm in an accessible and comfortable position for the operator. Make sure adequate lighting is available.

2. Apply a tourniquet above the point of entry and identify the basilic vein. The point of entry will be about 2 to 3 cm above the antecubital fossa and well around the medial aspect of the arm. Mark the point and release the tourni-quet but leave it in place.

3. Don gloves.

4. Clean the area thoroughly with iodine solution and drape it.

5. Open the catheter and measure the approximate length from the point of entry to the superior vena cava. A loose silk suture tied around the catheter can be used to mark the point. Fill the catheter with sterile saline or the solu-tion to be infused.

6. Infiltrate the area with lidocaine injected intradermally and subcutaneously.

7. A small skin incision at the needle entry site may be made at this point.

8. Have an assistant apply a tourniquet, already in place un-der the sterile drapes, without contaminating the field.

9. Connect the needle provided in the percutaneous CVP set to a 10-ml syringe filled with 2 to 3 ml of saline. Enter the vein with the needle. When a free return of blood is ob-tained, have the assistant release the tourniquet, discon-nect the syringe, and thread the catheter through the nee-dle. The catheter should be prefilled with the solution to be infused.

10. Once the catheter is introduced, advance it quickly to the

Technique 167

desired premarked distance. Delay in threading it may re-sult in vasospasm and render its further advancement more difficult.

11. Some difficulty may be encountered in advancing the cath-eter when it reaches the axilla. Have an assistant abduct the patient's arm (to straighten the junction of the basilic to the axillary vein) while gently rotating the catheter be-tween your thumb and forefinger.

12. Check the patency of the catheter by running the intra-venous solution and then lowering the intravenous bag or bottle below the level of the bed to check for free backflow of blood.

13. While holding the catheter in place, remove the needle. Remember, the catheter should never be withdrawn through the needle lest its end is accidentally sheared off by the sharp bevel edge of the needle, resulting in catheter embolization.

14. Secure the catheter in place with sutures. One suture at the point of entry will prevent movement of the catheter to and fro with consequent local irritation and infection. A more distal suture will serve as a double anchor and pre-vent kinking of the catheter.

15. Make a loop of the excess remaining part of the catheter and tape it to the skin.

16. Apply a generous dab of antibiotic ointment to the point of entry of the catheter into the skin. Clean the area again with iodine solution.

17. Apply a sterile occlusive dressing. Write the date of the dressing on the adhesive tape.

18. Obtain a chest roentgenogram to ascertain the position of the catheter.

C. Cutdown procedure In general the procedure is about the same as venipuncture, except that the vein is exposed and en-tered directly instead of the "blind" cannulation used for ve-nipuncture.

1. Identify the vein and prepare the area as for venipuncture (as above through step 6).

2. Make a transverse incision through the dermis into the subcutaneous tissue. The incision should be 3 cm proximal to the antecubital fossa and well around the inner or me-dial aspect of arm. This is a vascular area and the incision should be done carefully and just deep enough to reach the subcutaneous tissue, to avoid severing other vessels.

168 Central Venous Line Placement

3. Dissect the subcutaneous tissue bluntly with a hemostat in the direction of the vein. The purpose is to dissect the vein free from the subcutaneous tissue.

4. Once the vein has been freed, pass a curved hemostat un-der it to complete its dissection free from underlying sub-cutaneous tissue. Pull two ligatures with the hemostat un-der the vein.

5. Ligate the distal ligature securely. Do not cut the ends of the ligature; it will serve for control and traction of the vein. Leave the proximal ligature untied around the vein.

6. Applying traction on the distal tied ligature, make an oblique venotomy incision. The venotomy should not cut more than half the diameter of the vein. Either a blade or fine-pointed scissors may be used to cut the vein.

7. Introduce the catheter through the venotomy at right an-gles to the vessel wall before redirecting its tip forward into the vein. Toothed Adson forceps may be used to re-tract the lips of the venotomy and facilitate catheter inser-tion. If a beveled catheter is being used, make sure the sharp end of the bevel is cut off before insertion in order to avoid vessel wall injury or tear.

8. While maintaining traction on the distal ligature, advance the catheter quickly to the desired premarked distance.

9. Ascertain patency of the cannula (step 12 above). Tie the proximal ligature around the cannula. The tie should be tight enough to prevent backleak around it but not so tight as to prevent removal of the catheter when it is no longer needed.

10. Cut off excess suture material from the proximal and dis-tal ligatures. Close the skin around the catheter.

11. Secure the catheter to the skin and apply sterile occlusive dressing (steps 14 to 17 above). Follow the catheter care and removal procedures outlined under "Subclavian Vein Puncture" (steps 13 and 14 below).

12. Obtain a chest roentgenogram to determine catheter posi-tion.

SUBCLAVIAN VEIN PUNCTURE

The proximity of the subclavian vein to the undersurface of the clavicle, its caliber (2-cm diameter), and its fixed position (by sur-rounding structures) make it easily accessible for puncture. When puncture is properly done by a skillful operator, it is a fast and dependable means of establishing a central venous line. However, it is a blind procedure with inherent hazards; therefore

Technique 169

the potential of serious and fatal complications, particularly when it is performed by poorly trained, unskilled, and unsuper-vised individuals. Because of its possible grave sequelae, the pro-cedure must not only be indicated but it must be justified on the basis of the gravity or urgency of the patient's situation. In order to reduce the risk and increase the safety of the procedure in the hands of the beginner it should be done electively, after familiar-ity with the anatomy of the area, with strict attention to details of technique, and under expert supervision.

The subclavian vein starts at the outer edge of the first rib, passes through the angle formed by the rib and the medial third of the clavicle, and joins the internal jugular vein to continue as the innominate vein. It is one fingerbreadth anterior and medial to the subclavian-axillary artery junction. It has a large caliber and no valves, making it "representative" of right atrial pres-sures. It maintains a constant position by an investing fibrous tissue band attached to the rib and subclavian muscles. The in-fraclavicular approach is less likely to result in complications and is the one described here.

The left subclavian vein passes posterior to the clavicle near the junction of the inner and second quarters of the clavicle in the majority of patients. This is a more medial relationship than that which exists on the right side. The right subclavian vein passes posterior to the clavicle near the junction of its inner and middle thirds. The angle formed by the subclavian vein and the clavicle will vary with abduction of the arm and elevation of the shoulder. Puncture of the right subclavian vein rather than the left is preferred as this avoids the risk of damage to the thoracic duct.

A. Equipment

1. Sterile drapes, gloves, 4 x 4-in. gauze

2. Cleansing iodine solution

3. 14-gauge Intracath needle-cannula

4. Intravenous solution, tubing, three-way stopcock

5. 25-gauge needle, 10-ml syringes

6. 1 or 2% lidocaine solution

7. 25 ml of sterile saline

8. CVP manometer

B. Procedure

1. Position patient. The patient must be supine, with no pil-low under the head. A slight Trendelenburg position such that the neck veins are distended is preferred to prevent air embolism and dilate the subclavian vein for easier en-

170 Central Venous Line Placement

try. The patient's head is turned to the opposite direction This will make the landmarks more prominent, lessen the patient's anxiety of observing the operator, and prevent contamination caused by the patient's breathing on the equipment. The arms of the patient should be at the side The shoulders are thrown back and pulled up slightly, so as to flatten the anterior deltoid bulge, by a pillow or rolled towel under the back, between the shoulders.

2. Don gloves.

3. With the iodine solution, cleanse the entire medial two thirds of the clavicle extending to the midsternum and in-cluding the suprasternal notch.

4. Identify anatomical landmarks. Locate the junction of the medial and middle thirds of the clavicle. Mark the site of entry, slightly (1 cm) below this point, and infiltrate it subcutaneously with the local anesthetic.

5. Attach a 10-ml syringe, half-filled with saline, to the In-tracath needle. Make sure there are no air bubbles or air leak. Enter the skin at the previously marked point, with the needle at a 10- to 15-degree angle to the chest wall, its tip directed medially toward the posterosuperior angle of the sternal end of the clavicle. A good point of reference can be established by firmly pressing the opposite index finger into the suprasternal notch to locate the deep side of the superior angle of the clavicle and directing the course of the needle toward the fingertip. The course of the needle is through the pectoralis major muscle, upward over the first rib, and behind the clavicle to enter the sub-clavian vein near its junction with the axillary vein. Never change the needle direction without first withdraw-ing the needle to the skin. Changing the direction of the needle while it is in the deeper tissues may result in lac-eration of the vein.

6. After entry through the skin, inject 0.5 ml of saline to clear the needle of tissue plugs. Thereafter, a slight nega-tive pressure is maintained on the syringe while it is ad-vanced until a free flow of dark blood is returned. Now rotate the needle bevel caudally and advance it a few mil-limeters further to ensure clearance of the vein wall.

7. Order the patient to maintain a full inspiration, while you hold the needle steady with one hand and occlude it with one finger to prevent bleeding or air embolization; remove the syringe and thread the catheter through the needle and into the subclavian vein to a predetermined point be-yond the sternoclavicular joint.

Technique 171

8. Remove the guidewire for the catheter. When the catheter fills with blood, attach the infusion solution to the venous catheter and start the infusion.

9. While holding the catheter, remove the needle from the chest and apply a protective clip.

10. Secure the catheter to the skin with sutures. While one suture near the entry site is sufficient to prevent move-ment of the catheter in and out of the skin, a double an-chor (one at the puncture site and the other more distal) will help prevent kinking of the catheter.

11. Clean the skin again with iodine solution. Apply a gener-ous amount of a broad-spectrum antibiotic ointment to the entry site. Place a sterile occlusive dressing over the site. Date the dressing, on the adhesive tape.

12. Obtain an immediate chest roentgenogram to ascertain the exact position of the catheter and the absence of pneu-mothorax.

13. Catheter care. There should be daily aseptic changes of the administration set, extension tubing, and solutions. Carefully inspect the area for signs of inflammation, dis-charge, or local tenderness. Every 48 hours clean the puncture site and adjacent skin, apply antibiotic ointment, and cover the puncture site with an occlusive dressing. Record the time of change of the dressing.

14. Catheter removal. Clean the skin around the point of en-try with an iodine solution. Remove the catheter asepti-cally. Inspect the length of the extracted catheter. With sterile scissors clip its tip (2 cm) into a blood culture flask. Any discharge from the wound should be Gram-stained and cultured. Apply a Band-Aid to the puncture site. Strong consideration should be given to removing the catheter under following situations:

a. At first suggestion of local inflammation

b. Whenever any unexplained fever spike occurs

C. Whenever blood cannot be drawn freely, suggesting thrombosis at the tip

d. At the earliest date that the catheter is not essential to patient care

INTERNAL JUGULAR VENIPUNCTURE

This technique is now used preferentially in some centers. Its major advantages over subclavian venipuncture are the lower in-cidence of complications, specifically pneumothorax, and the fact

172 Central Venous Line Placement

that it presents a more direct route to the superior vena cava with a lower incidence of catheter malposition. Its disadvantages are the proximity of the vein to the carotid artery, and therefore the greater risk of arterial puncture, and the difficulty of using it in short-necked or obese patients. Its heretofore reported low rate of complications may be a reflection on its limited use by experts in its placement. It remains a blind procedure, with the potential for grave complications.

The internal jugular vein runs medial to the anterior portion of the sternocleidomastoid muscle in its upper part, in the trian-gle between the two inferior heads (clavicular, sternal) of the sternocleidomastoid muscle in its middle segment, and anterior to the clavicular head of the sternocleidomastoid muscle in its lower part. It runs in the carotid sheath close to the carotid ves-sels, the sympathetic chain, and the vagus and phrenic nerves. The right internal jugular vein is used in preference to the left because it is essentially a straight line to the right atrium and its puncture avoids the thoracic duct and higher pleural dome on the left.

A. Procedure The positioning of the patient, the equipment, and the technique of catheterization are identical to those of subclavian vein catheterization and will not be repeated here. The difference is in the point of entry and the vein utilized. Two different approaches to the internal jugular vein in rela-tion to the sternocleidomastoid muscle are available.

1. Central approach. The identifying landmarks are the ster-nal and clavicular attachments of the sternocleidomastoid muscle and the clavicle. The triangle formed by these is centered over the internal jugular vein. The needle is in-serted at the center of this triangle, at a 30-degree angle with the skin, and advanced caudally parallel to the sag-gital plane. The needle should never be directed medially, to avoid puncture of the common carotid artery. If initial entry is unsuccessful, withdraw the needle to under the skin, direct the needle point 5 to 10 degrees more later-ally, and readvance it while maintaining negative pres-sure with the syringe.

2. Posterior approach. The identifying landmarks are the sternocleidomastoid muscle at its crossing with the exter-nal jugular vein and the suprasternal notch. The site of skin puncture is along the lateral border of the sternoclei-domastoid muscle just above the point where the external jugular vein crosses it, at about 5 cm above the clavicle. The needle is advanced in a plane just below the sternO' cleidomastoid muscle directly toward the suprasternal notch, over which the operator places his left thumb in order to maintain orientation. This approach has a higher

Technique 173

risk of carotid artery puncture than the one described above.

To monitor the central venous pressure utilizing the central venous line placed by any of the three routes discussed above, use the following procedure:

1. Attach the CVP manometer with connecting tubing to the three-way stopcock in the intravenous line.

2. Determine the zero reference level. With the patient su-pine, a distance 5 cm below the sternal angle or 10 cm from the back, approximately at the anterior axillary line, corresponds to the level of entry of the superior vena cava into the right atrium. Clearly mark this point on the pa-tient's chest. This reference point must be constant in se-rial observations since the course of serial CVP values is more meaningful than a single CVP measurement.

3. With the patient supine, place the zero point of the ma-nometer with the zero reference level marked on the pa-tient's chest. If the patient is in the sitting position, a plane parallel to the floor and passing through the zero reference level is taken as the zero reading on the manom-eter.

4. Fill the manometer with 20 to 30 cm of solution from the intravenous infusion bottle.

5. Open the three-way stopcock so that the manometer is open to the central venous line going to the patient.

6. Allow the fluid to reach a steady state but fluctuating with respiration. The highest level of reading is taken as the CVP.

7. The reliability of the reading depends on the position of the catheter (checked with the chest roentgenogram) and patency of the central venous line. The line is considered to be uncompressed, unkinked, and open if:

a. Fluids can be injected and blood aspirated easily. If blood cannot be withdrawn from the catheter easily, the pressure measurements should be suspect. Flush the catheter or try to withdraw and reposition it.

b. There are free fluctuations of the fluid column with breathing and heartbeat. Lack of respiratory fluctua-tions indicates obstruction. Flush the line and repeat the measurement. Unusually active pulsations indicate right ventricular pressures. Withdraw the catheter gently for a few centimeters, flush it, and repeat the measurement.

174 Central Venous Line Placement

C. The fluid falls freely in the manometer. A step-like fall of the fluid column synchronous with the inspiration that usually occurs in the absence of free fluctuations suggests a ball-valve effect at the catheter tip and will result in a falsely low reading. Flush the catheter and repeat the measurement. If the problem persists, with-draw the catheter very slightly, flush it, and repeat the measurement. If this problem still persists, the catheter may have to be replaced.

d. There is free rise of the fluid column in the manometer with straining, coughing, or compression of the abdo-men. If these cannot be elicited, flush the line and re-peat the measurement. Positive-pressure breathing will augment the CVP and should be discontinued during CVP measurements.

IV. COMPLICATIONS It is virtually impossible to eliminate compli-cations of this procedure. With care, skill, and meticulous atten-tion to detail they can be reduced and circumvented but not ob-viated.

A. Infection Catheter-tip infection has been recorded in as few as 1% to 2% to as many as 60% of cases. The majority of or-ganisms cultured from catheter tips will be contaminants. The frequency of positive catheter-tip cultures and of infection is related to the length of time the catheter is in place; it can be minimized by early removal. Infected catheters are more com-mon in patients with infections preceding catheter placement, in whom the fibrin sleeves that form around the catheter ap-pear to harbor the infecting organism and seem to be little affected by antibiotics used. The incidence of infection is in-versely proportional to the experience of the operator and the care with which aseptic technique was followed in inserting the catheter. Rigorous aseptic techniques and the avoidance of unnecessary manipulation are the keystones to contamination control. The best method to prevent infection is to have an organized intravenous team trained in catheter care and in-sertion. A negative blood culture in the face of apparent sepsis should not absolve the catheter as the source of the sepsis. Use of intravenous piggyback medication or withdrawing of blood via a catheter is contraindicated in total parenteral nutrition and preferably in all other situations. No intravenous solution should be allowed to hang for longer than 24 hours.

If a catheter-related infection is suspected:

1. Clean the skin site with iodine solution.

2. Obtain aerobic and anaerobic cultures through the cathe-ter.

Complications 175

3. Remove the catheter aseptically. Clip 2 cm of its tip with sterile scissors into a blood culture medium.

4. Gram-stain and culture any purulent material from the puncture site.

5. If an infected solution is suspected, withdraw 20 ml of the fluid from the intravenous line. Culture 1 ml of this on a pour plate and place the remainder in a blood culture bottle.

B. Pneumothorax, hemothorax, and hydrothorax These are the most common (6%, 2%, and 1%, respectively) and poten-tially serious complications encountered. Inadvertent entry into the pleural cavity at the dome, in spite of the protection provided by the first rib, or laceration of the lung will result in some degree of pneumothorax. A postprocedure chest film is essential to determine size and therapy (needle aspiration or tube drainage). Laceration of the subclavian vein or artery will result in hemothorax, which may require surgical repair. Extraluminal insertion of the catheter tip into the pleural cavity will result in hydrothorax. Always ascertain free back-flow of blood prior to leaving the bedside and ordering fluid infusions.

C. Air embolism Air embolism, though very rare, is probably the most serious complication of this procedure. It can occur during insertion, when the needle is disconnected from the sy-ringe preparatory to catheter insertion, or it can occur when tube connections are disengaged and air is sucked into the ve-nous system because of negative intravenous pressure. The former can be prevented by having the patient in a 15-degree Trendelenburg position and in maximum inspiration for the brief period the needle is opened to air. The latter can be pre-vented by making sure all connections are firmly connected and secured.

D. Thrombosis, phlebitis, thrombophlebitis Sterile phlebitis is by far the most common complication of catheter placement, appearing within hours after insertion in some patients and increasing in frequency with the duration of catheterization. The large volume and high flow through the large-caliber veins used probably prevent an incidence higher than that ac-tually encountered. Subclavian and axillary vein thrombosis occur and are not prevented by anticoagulants. Suppurative thrombophlebitis is the most lethal form of complication, re-quiring immediate surgical therapy, if suspected.

It is not clear that either alkalinization of the fluids or the addition of heparin or steroids is helpful, but irritating drugs or fluids (hypertonic) should be avoided. Catheters should be discontinued as early as possible.

176 Central Venous Line Placement

E. Miscellaneous Less commonly encountered complications that have been observed are myocardial perforation, subcuta. neous hematoma or emphysema, brachial plexus injury, tho-racic duct laceration, phrenic nerve palsy, and clavicular os-teomyelitis.

V. INTERPRETATION The most important aspect of CVP interpre-tation is the realization of its limitations. The initial enthusiasm for the CVP was considerably dampened as subsequent studies revealed its unreliability as a true index of volume status.

Central venous pressure does provide a useful guide for fluid repletion. It does not reflect vascular volume per se, but rather indicates the relationship between the volume of blood that en-ters the heart and the effectiveness with which the heart ejects that volume.

It must be kept in mind that measurement of CVP is a mea-surement of pressure alone, not of volume. It is a function of sev-eral factors, including venous tone, volume status, and right ven-tricular function and compliance.

It has been shown repeatedly that measurement of pulmonary capillary wedge pressure is a much more accurate and reliable index to follow. In the normal patient there is a direct relation-ship between changes in CVP and changes in pulmonary capil-lary wedge pressure (the absolute values are dissimilar because of the differing compliance of the two ventricles). This is because the two healthy ventricles are "in phase" with respect to pres-sure-volume relationships. When disease affects one of the two ventricles, either acutely or chronically, they are thrown "out of phase" and the CVP and pulmonary capillary wedge pressure are no longer reliably related. Therefore, diseases that affect predom-inantly right ventricular function or compliance (cor pulmonale, pneumonia, pulmonary embolus) may be associated with high CVP readings and a low left ventricular filling pressure. Con-versely, left ventricular disease (acute myocardial infarction) may be associated with normal CVP readings and markedly ele-vated pulmonary capillary wedge pressure. Chronic left ventric-ular failure leads to right ventricular failure with elevated CVP and pulmonary capillary wedge pressure. However, changes in the CVP are not reliably related to changes in the pulmonary capillary wedge pressure in this situation.

Additionally, changes in venous tone may change the CVP ir-respective of volume status. The most common example of this is severe systemic acidosis (pH <7.20) that causes venoconstriction and elevated CVP in the face of normovolemia or hypovolemia.

The one situation in which the CVP is usually reliable is when it is very low (<2 cm H20) in association with arterial hypoten-sion. This usually denotes absolute or effective volume depletion (hemorrhage, sepsis, anaphylaxis). In these situations the central

References 177

venous line provides the additional advantage of easy access for fluid replacement or medication. When these situations are di-agnosed or suspected, CVP can be very helpful. With the CVP reading and the use of fluid challenge, one can "titrate" the pa-tient's right ventricular Starling curve. One recommended tech-nique is as follows:

Decide on a volume of fluid and infuse it over 10 minutes. The choice of fluid depends on the clinical situation. (A rough rule of thumb: if CVP < 1 0 cm H 2 0, give 200 ml; if CVP > 1 0 cm H 2 0, give 100 ml).

a. If the CVP rises more than 5 cm H 2 0 from the baseline value, stop the fluid challenge and observe the patient.

b. If the CVP rises more than 2 but less than 5 cm H 2 0 above baseline during the 10-minute infusion period, slow the infusion and wait 10 minutes. If the CVP then drops to within 2 cm H 2 0 of the baseline, resume the fluid challenge.

c. If the CVP does not rise more than 2 cm H 2 0 during the 10-minute infusion period, give another fluid load over 10 minutes.

d. Do not open the intravenous solution selected and come back a half-hour later to see what happened; fluid chal-lenges must be monitored closely and carefully.

The interpretation of the data obtained from this type of dynamic situation is much more reliable and useful than the absolute CVP value alone, particularly when these data are interpreted in the context of the clinical evaluation, i.e., improvement in mental status, increase in urine output, increase in the blood pressure, change in orthostatic pressure drop, pulse rate, respiratory rate, and the appearance of the skin of the extremities.

REFERENCES

Wilson J.N., Grow J.B., Demong C.V., et al.: Central venous pres-sure in optimal blood volume maintenance. Arch. Surg. 85:563-578, 1962.

The technique for continuous CVP monitoring is described (subcla-vian catheterization) and the usefulness of the procedure in differ-ent clinical settings is illustrated by 14 separate case histories. A good article. One of the first on the subject, it popularized the tech-nique.

Diedrick S., Wilmore D.: Long-term parenteral feeding. Hosp. Prac. 3:65-78, 1968.

To prevent infection, catheterization should be approached with the same care as a surgical incision. Once inserted, the catheter should

178 Central Venous Line Placement

not be used for other purposes. The more times the catheter tip disengaged from the infusion tubing and used to inject drugs or withdraw blood, the higher the risk of contamination and infection

Borja A.: Current status of infraclavicular subclavian vein catheter-ization. Ann. Thorac. Surg. 13:615-624, 1972.

A review of the English literature on subclavian vein catheterization highlighting the potential seriousness of the complications associ-ated with the procedure.

Land R.E.: Anatomic relationships of the right subclavian vein Arch. Surg. 102:178-180, 1971.

Right subclavian venograms were performed on 70 adults. Changes in anatomical relationships caused by abduction, shrugging, ro-tation of the head, and Trendelenburg's position are considered. In the supine positions with the arm at the side, the majority of right subclavian veins pass beneath the clavicle close to the junction of the inner and medial third of the bone.

Land R.E.: The relationship of the left subclavian vein to the clav-icle. J. Thorac. Cardiovasc. Surg. 63:564-568, 1972.

In the nonemergency situation, it is recommended that the vein be visualized fluoroscopically by injection of radiologic contrast mate-rial (25-ml bolus of 50% diatrizoate) into an ipsilateral antecubital vein.

Moosman D.A.: The anatomy of infraclavicular subclavian vein cath-eterization and its complications. Surg. Gynecol. Obstet. 136:71-74, 1973.

A good summary. Linos D.A., Mucha P., van Heerden J.A.: Subclavian vein: A golden route. Mayo Clin. Proc. 55:315-321, 1980.

A lucidly written, well-illustrated article on subclavian vein punc-ture.

Brahos G.J.: Central venous catheterization via the supraclavicular approach. J. Trauma 17:872-877, 1977.

A different route of entry into the subclavian vein. The lower rate of complications reported in this article reflects not the safety of the technique as such but the fact that all the procedures were done electively and under the direct supervision of the author.

James P.M., Myers R.T.: Central venous pressure monitoring: Mis-interpretations, abuses, indications and a new technic. Ann. Surg. 175:693-701, 1972.

The title speaks for itself. The new technique is that of the supra-clavicular approach to the subclavian vein.

Ng S.W., Rosen M.: Positioning central venous catheters through the basilic vein: A comparison of catheters. Br. J. Anaesth. 45: 1211-1214, 1973.

For catheterization of the superior vena cava or right atrium, 85.7% to 96.8% of catheters inserted through the subclavian vein could be positioned satisfactorily, compared with 39.6% and 70.3% (depending on the type of catheters used) of catheters passed through the basilic vein.

References 179

Daily P.O., Griepp R.B., Shumway N.E.: Percutaneous internal jug-ular vein cannulation. Arch. Surg. 101:534-576 , 1970.

Based on experience gained in use of the internal jugular vein for transvenous pacemaker insertion and peripheral cannulation for cardiopulmonary bypass, this technique was tried and found su-perior to subclavian vein catheterization for monitoring CVP dur-ing surgical procedures.

B r i n k m a n J.A., Costley D.O.: Internal jugular venipuncture. JA.MA. 223:182-183 , 1973.

An illustrated description of the technique. Defalque R.J.: Percutaneous catheterization of the internal jugular vein. Anes. Analg. 53 :116-121 , 1974.

A review of the procedure, its indications, complications, and technique.

Bernard R., Stahl W.: Subclavian vein catheterization: A prospective study: I. Non-infectious complications. Ann. Surg. 173:184-190, 1971.

In a prospective study of 202 subclavian vein punctures, the rate of noninfectious complications was 4.5%, with pneumothorax being the most frequent. All complications were the result of procedures performed by physicians relatively inexperienced (<50 catheteriza-tions) or unsupervised; about half the complications occurred in cases in which the procedure was regarded as an emergency (2% of patients).

Bernard R., Stahl W., Chase R.M.: Subclavian vein catheterizations: A prospective study: II. Infectious complications. Ann. Surg. 173:191-200, 1971.

In 98 subclavian catheters, the incidence of positive catheter cul-tures (40%) could be directly correlated with operator experience, repeated attempts at the procedure, and poor aseptic technique.

Herbst C.A.: Indications, management, and complications of percu-taneous subclavian catheters: An audit. Arch. Surg. 113:1421-1425, 1978.

A retrospective outcome-oriented audit of the procedure confirming the importance of physician inexperience as a cause of complica-tions: 46% of the complications occurred with physicians who had placed only one catheter. There was a 9.4% incidence of complica-tions on the surgical service, 14.3% on medicine, and 25% on gynecology.

Mitchell S. E., Clark R.A.: Complications of central venous cathe-terization. A.J.R. 133:467-476 , 1979.

A review of the complications of subclavian and internal jugular vein catheterization with emphasis on the radiologic findings.

Schapira M., Stern W.: Hazards of subclavian vein cannulation for central venous pressure monitoring. JA.MA. 201:327-329 , 1967.

The unfortunate experience of these authors with four cases dem-onstrating the dangers associated with subclavian vein catheteriza-tion leads them to suggest the abandonment of this technique.

Walters M.B., Stanger H.A.D., Roten C.E.: Complications with per-

180 Central Venous Line Placement

cutaneous central venous catheters. JA.MA. 220:1455-1457, 1972 In 240 cases of acute myocardial infarction, infection occurred rarely, phlebitis occurred in 16%, and 4 patients had symptomatic thrombosis; radiographic dye injection study on asymptomatic ax-illary vein thrombosis was considerably more frequent (25%). An-ticoagulant therapy was of no value in preventing thrombus for-mation.

Henzel J.H., DeWeese M.S.: Morbid and mortal complications asso-ciated with prolonged central venous cannulation: Awareness, rec-ognition and prevention. Am. J. Surg. 121:600-605, 1971.

In this review of four years' experience at one teaching center, com-plications could be directly attributed to two primary factors: a re-laxation of attitude toward critical points of catheterization as ex-perience was gained with the modality, and delegation of catheter care to inexperienced personnel.

Morgensen J.V., Frederiksen W., Jensen J.K.: Subclavian vein cath-eterization and infection: A bacteriological study of 130 catheter in-sertions. Scand. J. Infect. Dis. 4:31-36, 1972.

The risk of catheter infection is greater when subcutaneous subcla-vian catheters are inserted in patients who are infected before cath-eter insertion and with length of catheterization.

Maki D.G., Goldmann D.A., Rhame F.S.: Infection control in intra-venous therapy. Ann. Intern. Med. 79:867-888, 1973.

A detailed review of the subject, with an extensive bibliography. Hoshal V.: Intravenous catheters and infection.

A good summary of the "do's" and "dont's" of subclavian catheter placement and care.

Stein J.M., Pruitt B.A.: Suppurative thrombophlebitis: A lethal iat-rogenic disease. N. Engl. J. Med. 282:1452-1455, 1970.

The treatment of this complication of venous cannulation is sur-gical.

Lefrak E., Noon G.: Management of arterial injury secondary to at-tempted subclavian vein catheterization. Ann. Thorac. Surg. 14:294-298, 1972.

Immediate operative repair is the treatment of choice of any subcla-vian artery injury that results in production of a hemothorax.

Davison R., Cannon R.: Estimation of central venous pressure by examination of jugular veins. Am. Heart J. 87:279-282, 1974.

The CVP cannot be reliably estimated by inspection of the jugular veins. Only in 47% of observations was the estimation within 2 cm of the recorded value. To obtain a 90% coincidence, an error of up to 4 cm had to be allowed.

Longerbearm J., Vannix R., Wagner W., et al.: Central venous pres-sure monitoring. Am. J. Surg. 110:220-229, 1965.

A discussion of the importance of CVP monitoring as a guide to fluid therapy during shock and other forms of cardiovascular stress.

Shubin H., Weil M.H.: Routine central venous catheterization for management of critically ill patients, in Ingelfinger F.J., Ebert R.V.,

References 181

Finland M., et al. (eds.): Controversy in Internal Medicine. Philadel-phia, W.B. Saunders Co., 1974, vol. 2, pp. 1 7 7 - 1 8 5 . Swan H.J.C.: Central venous pressure as a n outmoded procedure of limited practical value, ibid, pp. 1 8 6 - 1 9 3 .

In these two articles the value and pitfalls of CVP monitoring are considered in this volume of controversies in medicine.

De Laurentis D., Hayes M., Matsumoto M., et al.: Does central ve-nous pressure accurately reflect hemodynamics and fluid volume patterns in the critical surgical patient? Am. J. Surg. 162:415-418, 1973.

Pulmonary artery pressures and pulmonary capillary wedge pres-sures more accurately reflect left ventricular function than do CVPs. The CVP and pulmonary pressure correlated in only 50% of 32 con-secutive surgical patients studied.

Mitchell J.H., Wildenthal K., Johnson R.L.: The effects of acid-base disturbances on cardiovascular and pulmonary function. Kidney Int. 1:375-389, 1972.

A good review of the effects of changes in pH on the "oxygen trans-port system" of the body.

15 Flow-Directed Balloon-Tipped (Swan-Ganz) Catheterization

I. INDICATIONS

A. Acute myocardial infarction In situations of continuous hemodynamic monitoring following acute myocardial infarc-tion where cardiac output is low and there is associated hy-potension and shock, catheterization will:

1. Identify patients who are hypovolemic and whose condi-tions can be expected to improve with volume expansion.

2. Help monitor hemodynamic changes during the acute phase of infarction.

3. Provide measurements indicative of poor prognosis.

B. Shock is an indication, particularly when its cause is not ap-parent or it is not readily reversible.

C. Hypovolemia Catheterization is indicated for the recognition of hypovolemia and the assessment of volume status of se-verely ill patients, as in acute pancreatitis, generalized peri-tonitis, decompensated cirrhosis, or severe trauma.

D. Fluid balance Catheterization is indicated for use in the management of fluid balance in noncardiogenic pulmonary edema, acute renal failure, noncardiogenic shock, and drug overdose.

E. In cases of respiratory failure of uncertain cause with persis-tent hypoxemia on a high forced inspiratory oxygen (FI02) in-dex, catheterization will help determine whether the cause of respiratory failure is cardiac or pulmonary.

F. Therapeutic interventions Catheterization is helpful in the assessment of hemodynamic effects and evaluation of thera-peutic interventions with vasoactive drugs, mechanical venti-lation, hemodialysis, and assisted circulation.

G. Evaluation of cardiac function Catheterization is indicated 182

Technique 183

to assist in the evaluation of cardiac function, particularly in ascertaining left ventricular function in the presence of known right ventricular dysfunction and in determining the presence of intracardiac shunts.

H. Cardiac surgery Assessment and monitoring of cardiovascu-lar function in the preoperative, intraoperative, and postoper-ative period in patients undergoing cardiac surgery and in procedures where major fluid shifts are expected may require catheterization.

I. Pulmonary angiography Catheterization may be used to in-ject contrast material for pulmonary angiography in cases of pulmonary embolization.

J. Research applications to obtain hemodynamic data on new or more traditional therapeutic interventions may require cath-eterization.

K. Administration of medication

II. CONTRAINDICATIONS There are no absolute contraindications to flow-directed pulmonary arterial catheterization. The presence of infective endocarditis, bleeding disorders, and tachyarrhyth-mias constitute relative contraindications.

Thus, the issue with the use of flow-directed catheterization should not be the absence of a contraindication but rather the need for precise hemodynamic data that cannot be obtained from the noninvasive clinical evaluation of the patient's condition.

Due to the relative simplicity of flow-directed catheterization, users tend to underestimate the cost and potential for serious complications that pertain to all invasive procedures. This is a costly and invasive procedure that is certainly not innocuous. In each and every case the risks and cost must be weighed against the potential benefits.

III. TECHNIQUE

A. Equipment includes standard cutdown set, strain-gauge pres-sure transducer with connecting tubing and three-way stop-cock, pressure recorder, ECG monitor, defibrillator, syringes, sterile saline, heparinized solution for constant infusion and priming of catheter, lidocaine, and balloon-tipped catheter.

Since the catheter's introduction in 1970, as a double-lu-men, balloon-tipped, flexible polyvinyl catheter, a host of cath-eters have become available.

1. 5-F double-lumen catheter with single end-hole

a. Advantage Can be inserted through No. 14 intra-medicut transcutaneously, obviating cutdown.

184 Swan-Ganz Catheterization

b. Disadvantage Not suitable for long-term use due to its small lumen size.

C. Indications Diagnostic evaluation, particularly to sep-arate cardiogenic from noncardiogenic edema, to ascer-tain presence of left-sided heart dysfunction, etc.

2. 7-F double-lumen catheter with single end-hole

a. Advantage Larger lumen makes catheter obstruction less likely. It can be inserted transcutaneously with guidewire and introducer.

b. Disadvantage It usually requires cutdown, and does not allow access to right atrium for pressure monitoring or blood sampling.

c. Indications As above, and for longer-term evaluation of responses to therapy, etc.

3. 7-F triple-lumen catheter with end-hole and side-hole 20 to 30 cm proximal to catheter tip

a. Advantage Access to right atrium for pressure moni-toring and blood sampling.

b. Disadvantage Requires cutdown.

c. Indications As in item 2, evaluation of right-sided heart failure by monitoring right atrial pressure (equiv-alent to right ventricular end diastolic pressure).

4. 7-F triple-lumen catheter with end-hole and side-hole as above and thermistor at distal tip

a. Advantage As in item 3; also, this catheter permits determination of cardiac output by thermodilution.

b. Disadvantage As in item 3.

c. Indications To ascertain cardiac output directly rather than inferentially from the arteriovenous oxygen con-tent difference, usually in cases of septic shock or shock with acidosis.

B. Catheter insertion

1. The catheter may be inserted through a cutdown in the antecubital fossa or by percutaneous venipuncture of the subclavian, basilic, or internal jugular veins. For details of these procedures, see chapter 15.

2. The shafts of the catheters are marked to indicate 10-cm distances from the catheter tip. For the average person, advancement of 35 to 40 cm from the right and 45 to 50 cm from the left antecubital fossae should place the cath-eter tip in or close to right atrium. If subclavian or inter-

Technique 185

nal jugular venipuncture is used, the right atrium is 10 to 15 cm from the internal jugular vein and 10 cm from the subclavian vein.

3. Prior to insertion of the catheter, test the balloon for leaks. With the balloon submerged in a cup of sterile sa-line, inflate it with 0.8 to 1.0 cc of air by way of the small side catheter connected to a 1-ml syringe. The connector to the 1-ml syringe is identified by a different color. De-flate the balloon. Flush and fill the catheter with heparin-ized solution and attach it to the heparinized solution (1,000 units in 250 ml of 5% dextrose in water) to be used in flushing.

4. Insert the catheter in the vein. Use sterile operative pro-cedures. Don sterile gown, gloves, mask, and cap. For technique, see chapter 15. Insert the needle and sheath together, then withdraw the needle and insert the catheter through the sheath. Perform aspiration of blood to confirm intravenous placement as soon as the catheter tip is through the sheath; then flush the catheter and open it to the transducer. For percutaneous insertion:

a. Use 5-F catheter with No. 14 intramedicut or Edslab catheter introducer No. 9701.

b. Use 7-F catheter with Edslab catheter introducer No. 9702. The percutaneous needle for the 7-F catheter is very large and probably should not be introduced into the subclavian or jugular veins.

C. A No. 8 Cordis introducer may also be used for insertion of a No. 7 catheter. (1) Begin intravenous solution via sterile puncture of a

medial anticubital vein with a No. 16 (or No. 14) medicut. Slip guidewire through the plastic sheath and then remove the catheter completely. Place the white plastic introducer over the blue guide catheter and slide both over the wire gently, introducing them both into the arm vein as far as the hub will allow. Remove the guidewire and inner blue sheath and check for blood flow. Often a small nick is re-quired in the skin to facilitate entry. Do not anes-thetize the area over the vein until at least the guidewire is in place. The Swan-Ganz catheter may then be slipped through the white catheter into place as described.

(2) It is extremely important to remember that finesse rather than force is the key to successful catheter placement. Often, gentle rotation of the catheter with an in-and-out motion will facilitate movement of the tube through difficult venous passages.

186 Swan-Ganz Catheterization

Fig 16-1.—Pressure tracings (top) and values (bottom) obtained during advancement of Swan-Ganz catheter. RAP indicates right atrial pressure; RVP, right ventricular pressure; PAP, pulmonary artery pressure; PAWP, pulmonary artery wedge pressure; and LVP, left ventricular pressure. Bar over number indicates mean pressure readings; numbers in parentheses indicate range of pressure. Values are given in millimeters of mercury.

Technique 187

(3) This technique may also be used with a subclavian needle for insertion of the catheter into the subcla-vian vein.

5. Advance the catheter. Open the catheter to the transducer and advance it under continuous pressure and ECG mon-itoring (Fig 16-1) . Watch for an increase in pressure variations associated with respiratory cycle. This will in-dicate that the tip of the catheter is within the thorax. At this point cough will produce a deflection of 40 mm Hg in the pressure recording. Where possible, ask the patient to cough to ascertain this.

If an antecubital vein is used and the catheter does not traverse the veins in the axilla with ease, inflate the bal-loon with 0.4 to 0.6 cc of air and withdraw the catheter slightly before further advancement. The inflated balloon will help float the catheter along the blood flow current to the superior vena cava. The balloon should not be fully inflated in order to avoid injury to the smaller-sized ves-sels it might be traversing.

6. As soon as the display scope shows respiratory variations of pressure, inflate the balloon with 0.8 cc of air and allow it to proceed downstream, while the ECG is being moni-tored and the pressures are being recorded, until pressures resembling pulmonary-artery wedge pressures are ob-tained. Deflate the balloon.

This part of the procedure should usually last only a few seconds. Monitor the ECG very closely so as to promptly detect disturbanes of cardiac rhythm that might be asso-ciated with passage of the catheter through the cardiac cavities.

a. The catheter will fail to enter the pulmonary artery in 5% of cases. Failure is usually due to severe pulmonary hypertension, very low cardiac output states, or valvu-lar disease.

If the catheter does not readily wedge when initially floated in with the balloon inflated, deflate the balloon, pull the catheter back to the right atrium or superior vena cava, reinflate the balloon, and push the catheter forward until it wedges. Failure to wedge is usually due to looping of the catheter within a cardiac chamber and should be suspected when more than the expected length of catheter has been advanced without obtaining a wedge pressure.

b. Inflate the balloon as soon as a large-caliber vein is en-countered and float it into the pulmonary artery. On inflation, the balloon surface becomes flush with the catheter tip, such that the rigid tip does not protrude

188 Swan-Ganz Catheterization

past the inflated balloon surface. When the balloon is deflated, the rigid catheter tip is exposed and can irri-tate the right ventricle, with resultant arrhythmias. Also, the inflated balloon will not allow the tip of the catheter to proceed too far peripherally, thereby reduc-ing the likelihood of pulmonary vascular complications.

c. Do not use water or saline to inflate the balloon. The small lumen of the balloon makes it difficult to deflate when filled with fluid and therefore difficult to with-draw without valvular or vascular injury. Also, the weight of the liquid will impede the flow or flotation of the balloon into a distal capillary. If a shunt is sus-pected and there is any possibility of the catheter pass-ing into the left side of the heart, carbon dioxide should be used to inflate the balloon.

d. To check for adequate wedging, use the following cri-teria: (1) Pulmonary artery phasic contour should change to a

left atrial tracing (see Fig 16-1) . (2) Mean wedge pressure should be less than mean pul-

monary artery pressure. (3) Blood withdrawn from wedge position should be

fully oxygenated, except in the presence of a shunt. (4) Use chest films to confirm the position of the cathe-

ter. Actually, although one advantage of the bal-loon-tipped flotation catheter is its use at the bed-side, whenever possible and available fluoroscopic assistance should be employed.

e. As soon as the balloon is deflated, pulmonary artery pressure tracings should be seen again.

7. Secure the catheter to the skin with sutures, apply a broad-spectrum ointment at the point of entry into the skin, cover the point of entry with an occlusive dressing, and follow catheter care and removal procedures as de-scribed in chapter 15.

8. Once the catheter is secured, a pulmonary arterial (PA) blood sample, a right atrial blood sample, and an arterial sample are obtained and C(a-v)02 is calculated for esti-mation of cardiac output. The proximal catheter lumen is usually in the right atrium (RA). RA blood is obtained to be sure that the PA sample is not artificially elevated due to contamination with "wedge" blood, i.e., blood directly in contact with an alveolus.

9. Obtain chest roentgenogram immediately to confirm cath-eter position and rule out complications. Thereafter, ob-tain daily chest films to check for catheter position and possible catheter complications.

Technique 189

10. The frequency of pressure readings will depend on the instability of the patient. Between pressure measurements maintain a constant heparin flush: 1,000 units of heparin in 5% dextrose in water to run over 24 hours.

11. Evaluate the character of the tracing repeatedly, with the balloon deflated and the catheter adequately flushed. Loss of the characteristic phasic pulmonary artery tracing sug-gests that the tip of the catheter has advanced peripher-ally and totally occluded a pulmonary artery segment. The catheter has a tendency to slip into a persistent wedge po-sition under the pulsatile propelling force of the blood flow. Also, during the first 12 hours, the loop formed by the catheter as it traverses the cardiac chambers into the pulmonary artery tends to become smaller, causing the end of the catheter to be propelled into the smaller pul-monary artery branches. Wedging of the uninflated cath-eter is an undesirable eventuality that will result in pul-monary vascular injury and should be watched for.

12. To obtain wedge pressures, inflate the balloon under con-stant pressure monitoring. Stop inflation as soon as the character of the tracing indicates that the wedge position has been obtained. Limit wedging time to a maximum of two to three respiratory cycles or 10 to 15 seconds in order to minimize pulmonary vascular wall stress. Once the wedge pressure has been obtained, deflate the balloon. Al-ways inflate the balloon gradually to avoid overdistention of the pulmonary artery. If wedge pressures are obtained with volumes less than indicated on the catheter shaft (0.8 cc for 5-F and 1.5 cc for 7-F), it is probable that the cath-eter has advanced too far and it should be partially with-drawn. Inflation of the balloon should produce a feeling of resistance and, on release of pressure, the barrel of the syringe should slip back. If no resistance is encountered, question the integrity of the balloon and discontinue fur-ther inflation.

To avoid balloon rupture, before each "wedge" reading aspirate the balloon to assure complete emptying prior to its inflation for the reading.

13. If no pressure tracings can be obtained, the catheter may be clotted or the stopcock may be turned in the wrong di-rection. The latter is easy to correct. If it is a clot, try to aspirate it and then flush the catheter. Do not flush the catheter if blood cannot be aspirated. Usually, a clot will be heralded by "damping" of the pressure tracing. Flush-ing at this time is indicated and will prevent clotting.

14. If the PA diastolic pressure has been determined to be equal to the pulmonary capillary wedge pressure, this in-dex may be used to follow hemodynamics rather than the

88 Swan-Ganz Catheterization

pulmonary capillary wedge pressure. This will prove more accurate in the long run and will eliminate unnecessary manipulation of the catheter, possibly preventing compli. cations. It has been demonstrated that in the absence of severe lung disease (a pulmonary artery diastolic-pulmo-nary capillary wedge gradient less than 5 mm Hg) the PA diastolic pressure will accurately reflect left atrial and therefore, left ventricular filling pressures.

C. Principles of calibration Although the equipment used is not uniform, certain guidelines can be given.

1. Pressure transducers should be balanced against a fluid system. Some transducers are used with disposable sterile domes with plastic membranes. Water may or may not be needed between the transducer itself and the plastic mem-brane; ascertain the requirements of each individual transducer and use it accordingly. However, the dome it-self should be filled with fluid and should be free of air bubbles.

2. A vacuum should not be created on the transducer surface as this may irreparably damage it, i.e., do not create neg-ative pressure (less than atmospheric) against the trans-ducer with a syringe.

3. Most of the pressure modules require balancing with the transducer open to air, i.e., at zero pressure. For this bal-ancing, the transducer should be at the level of the atrium. Electrical calibration can then be performed.

4. Since electrical calibration of some of the equipment is not stable, direct calibration with a mercury manometer should also be performed. This requires a blood pressure manometer and a stopcock system set up so that pressure can be exerted from an air-filled syringe simultaneously on the transducer and the manometer.

As pressure is changed with the syringe, this should be reflected on the oscilloscope of the pressure monitor, per-mitting exact calibration.

5. It is crucial that no leaks be present in this system or all readings will be inaccurate.

6. Loosening of the dome of the transducer will result in damping or loss of the pressure tracing. When this occurs, blood will leak back into the transducer. Tighten the dome of the transducer and flush the catheter to correct it.

Complications 191

IV. COMPLICATIONS A. Mechanical

1. Stiffness in the Shoulder due to restriction of arm move-ment and irritation along the course of the vein is a com-mon nuisance that will respond to mild analgesics.

2. Equipment malfunction with consequent incorrect data acquisition It is important to know what data to expect, to know what is correct, and to understand its signifi-cance. See the following section on Interpretation.

3. Balloon rupture The latex balloon absorbs lipoproteins and with prolonged indwelling loses its elasticity, thereby increasing the possibility of its rupture. Rupture will re-sult in embolization of air or balloon fragments. Care-ful adherence to technique should prevent this complica-tion.

4. Intracardiac knotting of catheter This is more likely to occur with smaller catheters. It can be avoided if no more than 10 cm of catheter is introduced while the catheter remains in either the right atrium or the right ventricle.

5. Loss of catheter Avoid manipulation of the catheter and anchor it to the skin at the point of entry.

B. Cardiac

1. Arrhythmias These are usually premature ventricular contractions that occur when passing the pulmonic valve, particularly if the balloon is not inflated and the rigid catheter tip irritates the right ventricle. More rarely, the catheter may recoil into the ventricle or the pulmonary valve area and cause arrhythmias. Therapy is rarely re-quired, but a defibrillator and lidocaine should be imme-diately available.

2. Heart block Right bundle-branch or complete heart block is a very rare complication.

3. Rupture of chordae tendineae of tricuspid valve is an ex-tremely rare complication reflecting poor technique: undue manipulation of the catheter without the use of fluoros-copy.

4. Endocardial mural thrombi may form in the presence of a hypercoagulable state or following prolonged catheteriza-tion.

5. Cardiac tamponade due to ventricular wall rupture The balloon should always be inflated when going through the cardiac chambers.

192 Swan-Ganz Catheterization

6. Endocarditis Poor catheter care or unsterile technique will be complicated by endocarditis, particularly in a se-verely ill patient.

C. Pulmonary 1. Pulmonary embolization may occur from venous thrombi

developing around the catheter or its tip or from rupture of the balloon, with consequent air or balloon fragment embolization.

2. Thrombosis of major pulmonary vessel around catheter Avoid prolonged catheterization and catheter manipulation. If a hypercoagulable state exists, consider anticoagulation.

3. Pulmonary infarctions are usually small, asymptomatic, and detected only on careful scrutiny. Pulmonary infarc-tion may result from any one of the following: thrombus formation around the catheter either peripherally or more proximally in the pulmonary artery; thrombus formation within the catheter; occlusion of a branch of the pulmo-nary artery by the wedging of the catheter tip; or leaving balloon inflated after a wedge reading.

4. Pulmonary artery perforation is probably the single most serious complication of this procedure. Careful adherence to technique with advancement of the catheter only when the balloon is inflated should prevent this potentially fatal complication. Rupture of a pulmonary vessel may occur if the catheter is already wedged when the balloon is in-flated. Under such circumstances, inflation will cause de-viation of the tip of the catheter into the arterial wall with resultant perforation of the vessel, hence the importance of inflating the balloon under constant pressure monitor-ing. Cardiac pulsation might also lead to shearing the catheter tip against the wall of the pulmonary artery.

D. Thrombotic As with all indwelling catheters, the potential for thrombosis and/or thrombophlebitis is a real one. Always examine the extremity for signs of thrombophlebitis and re-move the catheter at the earliest evidence thereof.

E. Infections

1. Bacterial endocarditis is a rare occurrence which must be watched for and considered in the differential diagnosis of any febrile episode that might develop.

2. Localized infection at site of catheter insertion (see chap-ter 15).

3. Sepsis With sterile insertion technique and careful cath-eter handling, this should be a preventable complication (see chapter 15).

Interpretation 193

V. INTERPRETATION The rational use of the Swan-Ganz catheter requires knowledge and understanding of several physiologic concepts: A. Cardiac function curves

1. With a normal myocardium, the greater the filling pressure the higher the cardiac output, until a point at which further increments in pressure no longer alter the output.

2. With abnormal myocardium, increments in filling pres-sure will increase output to an adequate level, but output is lower for any given filling pressure.

3. Myocardial function may be so poor that even a greatly augmented pressure will not result in adequate output.

4. Changing the function of a given heart from one curve to another requires a change not in volume or pressure, but in inotropic forces. Inotropic agents may be endogenous (acidosis, catecholamines) or exogenous (digoxin, catechol-amines, pressors).

5. In acute myocardial infarction, damage to heart muscle may be sufficient that pulmonary capillary wedge pres-sures of up to 18 mm Hg may be required for adequate output. In such a patient, the filling pressures should be increased to this level before it is concluded that an ade-quate output will not occur.

6. In a very poorly compliant heart, small increases in vol-ume may result in larger increases in pressure so that even at high filling pressures, output remains low.

B. Pulmonary water transfer Under normal circumstances, fluid remains in vessels because of a balance between hydro-static pressure pushing fluid out and colloid oncotic pressure pulling fluid in. The normal values for these are 5 to 12 cm H 2 0 pulmonary capillary (PCW) and 20 to 25 cm H 2 0 colloid oncotic pressure (COP), so that the COP-PCW gradient is 8 to 20 cm H 2 0. Maintenance of this gradient assures dry lungs unless primary capillary drainage is present. The more dis-turbed the gradient, the more likelihood that pulmonary edema will occur. In general, the tissue oncotic pressure and hydrostatic pressure are major determinants of fluid transfer, although they do influence the distribution of extravascular fluid within the lung parenchyma.

The COP depends mainly on albumin levels and, to a lesser extent, globulin levels. Pulmonary edema will occur at a much lower PCW with the low COP than with normal COP. The rationale for the use of salt-poor albumin in such patients is to increase the COP and thereby pull fluid back into the vas-cular system or prevent its egress.

194 Swan-Ganz Catheterization

C. Cardiac output As is apparent from the above discussion, in. creases in PCW lead both to improvement in cardiac output and to pulmonary edema. It is, therefore, necessary to balance the PCW and COP to maximize cardiac output and minimize edema. Clinically, we usually estimate the level of cardiac output (CO) from the use of the Fick equation:

CO = v o -( a - v ) 0 2

where V 0 2 represents oxygen consumption and (a - v) 0 2 rep-resents arteriovenous oxygen content difference.

The assumption is made that V 0 2 is relatively normal and is constant. One can then conclude that a high (a - v) 0 2 indi-cates a low CO and vice versa, and that any change in ( a - v ) 0 2 implies an opposite change in CO.

Under certain circumstances, V 0 2 cannot be assumed to be constant or normal. These include shock with lactic acidosis and gram-negative sepsis. In these situations, measure CO di-rectly; usually this is most readily done by inserting a ther-modilution cardiac output Swan-Ganz catheter initially and measuring CO as well as ( a - v ) 0 2 and pressures.

D. Miscellaneous interpretations

1. Pulmonary artery pressures and relationships The pul-monary arterial systolic pressure is a function of the state of the right ventricle and, to a lesser extent, the pulmo-nary vasculature. Under normal circumstances, the dia-stolic pressure is determined by the PCW. Since the pul-monary vascular resistance is normally quite low, the pul-monary diastolic pressure and the PCW are almost equal, with at most a gradient of 5 cm H 2 0. When the pulmonary vascular resistance is increased, the gradient between the diastolic pressure and the PCW widens, and this is, there-fore, pathognomonic of pulmonary vascular disease. Chronically, this is most common with chronic obstructive pulmonary disease; acutely, it may be due to pulmonary emboli, adult respiratory distress syndrome (ARDS), etc.

2. ARDS In a significant number of patients with pulmo-nary edema, pressure determinations are normal, as is COP and CO. In such patients an alternative explanation for pulmonary edema must be present. By definition, the ARDS is due to damage to the alveolar capillary. Here, regardless of pressures, fluid can leak from the vessels into the lungs due to separation of cell junctions, producing functional "holes" in the vessel. Attempts to manipulate PCW and COP in this situation should be tried but results are less predictable. For example, if administered albumin freely crosses from intravascular to extravascular spaces,

References 195

it may increase tissue oncotic pressure and pull H 2 0 with it, actually worsening pulmonary edema. When this oc-curs, various respiratory maneuvers, especially the use of positive end-expiratory pressure, are tried in an attempt to maintain life until healing can occur.

Evaluation of the degree of lung disease is made by the calculation of intrapulmonic shunting and by observing changes in the shunt fraction (QS/QT) with therapeutic ma-neuvers.

The shunt equation (measured while the patient is breathing 100% oxygen) is as follows:

_ C cap 0 2 - C art P 2

C cap 0 2 - C ven 0 2

where QS/QT represents the percent of CO not flowing by ventilated alveoli and C cap 0 2 represents the content of capillary blood for oxygen.

In the presence of a Qs/Q,r greater than 40%, there will be minimal response to changes in inspired oxygen and the patient should be maintained on the lowest FI0 2 con-sistent with a Pa0 2 greater than 50 mm Hg:

% sat Content = (Hgb x 1.34 x + (Po2 x 0.003)

C cap = (Hgb x 1.34) + (Pa02 x 0.003)

where Hgb represents hemoglobin in mg/dl and % sat, per-cent oxygen saturation.

In the presence of a significant increase in QS/QT, the venous Po2 becomes an important determinant of Pa02 . Since the venous Po2 is determined predominantly by car-diac output, a low cardiac output will, therefore, worsen any degree of hypoxemia.

REFERENCES

Swan H.J.C., Ganz W., Forrester J., et al.: Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N. Engl. J. Med. 283:447-451, 1970.

Original description of the technique, value, and clinical applica-bility of the procedure to the care of patients in the intensive care and coronary care units. In 60 attempts to pass the catheter in 37 patients, pulmonary arte-rial pressure was obtained successfully in 95% and pulmonary wedge pressure in 72%. Premature ventricular contractions oc-curred in 11%.

Swan H.J.C., Ganz W.: Use of balloon flotation catheter in critically ill patients. Surg. Clin. North Am. 55:501-520, 1975.

A well-written, easy-to-read comprehensive summary outlining the

196 Swan-Ganz Catheterization

technique, measurements obtained, and their application to dis-ease states.

Swan H.J.C., Ganz W.: Guidelines for use of balloon-tipped catheter Am. J. Cardiol. 34:119-120, 1974.

The "do's" and "dont's" for the safe use of the balloon-tipped cathe-ter are listed.

Carrico C.J., Horowitz J.H.: Monitoring the critically ill surgical pa-tient. Adv. Surg. 11:101-127, 1977.

A brief but practical overview of the commonly used devices in mon-itoring the conditions of critically ill patients.

Adams N.R.: Reducing the perils of intracardiac monitoring. Nurs-ing, April 1976, pp. 6 6 - 7 4 .

Written for nurses, this is a cleverly done photostory on how to care for the Swan-Ganz catheter.

Dalen J.E.: Bedside hemodynamic monitoring. N. Engl. J. Med. 301:1176-1178, 1979.

A thoughtful and concerned editorial on the cost, complications, and probably inappropriate overutilization of the technique.

Foote G.A., Schabel S.I., Hodges M.: Pulmonary complications of the flow-directed balloon-tipped catheter. N. Engl. J. Med. 290:927-931, 1974.

A retrospective analysis of the course of 125 catheterized patients showing that in 9 (7.2%), pulmonary ischemic lesions appeared to have occurred as a direct result of the use of the Swan-Ganz cathe-ter.

Pape L.A., Haffajee C.I., Markis J.E., et al.: Fatal pulmonary hem-orrhage after use of the flow-directed balloon-tipped catheter. Ann. Intern. Med. 90:344-347, 1979.

A report of five cases (encountered in a 2-year period in four hospi-tals) of what is probably the single most serious complication of the use of the flow-directed catheter. Associated predisposing factors are advanced age, pulmonary hypertension, and anticoagulation.

Pace N.L.: A critique of flow-directed pulmonary arterial catheteri-zation. Anesthesiology 47:455-465, 1977.

A critical evaluation of the data derived from the use of the flow-directed balloon flotation catheter emphasizing the inherent limita-tions in pulmonary arterial monitoring.

Scott M.L., Wehre D.R., Arens J.F., et al.: Clinical application of a flow-directed balloon-tipped cardiac catheter. Am. Surg. 38:690-696, 1972.

The experience with 123 patients at one center is summarized. Pontoppidan H., Laver M.B., Gettin B.: Acute respiratory failure in the surgical patient. Adv. Surg. 4:163-254, 1970.

A successful attempt to present simply the rather complicated hemo-dynamics of normal and abnormal respiratory pathophysiology.

Ramo B.W., Myers N., Wallace A.G., et al.: Hemodynamic findings in 123 patients with acute myocardial infarction on admission. Cir-culation 42:567-577, 1970.

Hemodynamic findings generally correlated well with the clinical

References 197

status of the patient. However, within each clinical class of patients (congestive heart failure, pulmonary edema, shock) there was a wide spectrum of values for each measurement, with considerable overlap of the values found within each clinical classification, such that hemodynamic evaluation of the conditions of patients with acute myocardial infarction presents a profile that is frequently dif-ferent from that presented by the clinical evaluation alone.

Ratshin R.A., Rackley C.E., Russell R.O.: Hemodynamic evaluation of left ventricular function in shock complicating myocardial infarc-tion. Circulation 45:127-138, 1972.

Hemodynamic evaluation can provide prognostic information in acute myocardial infarction. In this study of 22 patients, the mor-tality was 100% whenever the pulmonary arterial end diastolic pressure or left ventricular end diastolic pressure was over 28 mm Hg or over 15 mm Hg in association with a cardiac index of less than 2.3 L/min/sqm.

17 Pericardiocentesis

I. INDICATIONS Needle aspiration of the pericardium is a useful therapeutic and diagnostic procedure. It is, however, a major pro-cedure, and even in the best of hands it is fraught with serious and even fatal complications. In inexperienced hands it is a haz-ardous procedure. Therefore, except in cases of emergency, it should be performed only by or under the direct supervision of a physician well experienced in the technique. Pericardiocentesis should not be used simply to determine the presence or absence of pericardial fluid. It should be undertaken only after the pres-ence and extent of pericardial effusion has been determined on the basis of the clinical picture, the chest roentgenogram, and the ECG and confirmed by echocardiography.

A. Therapeutic in acute cardiac tamponade Cardiac tampon-ade results either from rapid rises of intrapericardial pressure that do not allow t ime for compensation or when the compen-satory mechanisms have been exhausted. The size of the pericardial effusion does not necessarily correlate with its functional import. The pericardium can easily accommodate 80 to 100 ml of fluid; after this, if the accumulation of fluid is slow (weeks or months) the pericardial sac will distend to ac-commodate several liters of fluid without necessarily resulting in cardiac tamponade. On the other hand, the rapid accumu-lation of as little as 150 ml (myocardial laceration, aortic dis-section) can result in potentially fatal tamponade within min-utes because of the preponderance of tough fibrous t issue and the relative sparsity of elastic tissue in the pericardium.

The dramatic relief that follows the removal of pericardial fluid in cardiac tamponade makes pericardiocentesis not only a l ifesaving procedure but one of the most rewarding experi-ences in clinical medicine. In every patient in whom pericar-dial effusion is suspected or documented, it is absolutely es-sential to monitor the patient for signs of cardiac compression and to be prepared to perform a therapeutic pericardiocen-tesis. The signs to watch for are:

1. Cyanosis, dyspnea, shock-like state, loss of consciousness

1 9 8

Contraindications 199

2. Rising peripheral (>130 mm H 20) or central (>200 mm H 20) venous pressure

3. Pulse pressure less than 20 mm Hg

4. Pulsus paradoxus greater than 50% of the pulse pressure B. Diagnostic A sample of pericardial fluid, adequately exam-

ined, will confirm the diagnosis or establish the underlying cause of the effusion, particularly when acute bacterial peri-carditis or malignant effusion are considered as the possible cause of the effusion. This is an elective procedure and should be performed under conditions that will yield the maximum information. It is in these conditions that open pericardiotomy has been advocated as the more direct approach.

In some centers, except in acute cardiac tamponade, a sur-gical approach such as anterior subxiphoid pericardiectomy, is favored as the diagnostic procedure of choice because of its greater safety, higher frequency of successful drainage, and its ability to provide pericardial tissue for histologic diagnosis. The fact remains that pericardiocentesis is the more conve-nient and easier procedure in the initial evaluation and man-agement of pericardial effusions, particularly when venous pressures are elevated and the patient's condition is debili-tated or the patient is a poor surgical risk. In any case, except in emergencies, the procedure should be performed by or un-der the supervision of an experienced individual, in a setting in which maximum diagnostic and physiologic information can be obtained and where surgical assistance is immediately available.

C. Instillation of therapeutic agents The intrapericardial instil-lation of a number of agents (nitrogen mustard, thiotepa, tet-racycline, radioactive chromic phosphate) has been effectively used in the therapy for neoplastic pericardial effusions. The instillation of a nonreabsorbable steroid has been shown to be effective in the treatment of dialysis-associated pericarditis encountered in patients receiving long-term maintainance di-alysis. These modalities of treatment are best done by leaving a plastic catheter in the pericardial space, both to provide drainage and to permit repeated drug instillation.

II. CONTRAINDICATIONS There are no absolute contraindications to pericardiocentesis, particularly in the presence of evidence of cardiac tamponade or progressive signs of cardiac compression.

The presence of a bleeding abnormality—prolonged prothrom-bin time or a low platelet count (<50,000/cu mm)—constitutes a relative contraindication that except in an emergency, should be corrected prior to attempting pericardiocentesis.

200 Pericardiocentesis

Fig 17-1.—Pericardiocentesis using ECG monitoring. Inset, point, angle, and direction of entry.

III. TECHNIQUE Pericardiocentesis is done with continuous ECG monitoring of the aspiration needle, which may be inserted using one of two approaches: subxiphoid or apical (Fig 17-1) . The subxiphoid approach avoids entrance into the pleural space, ap-proaches the posterior portion of the right ventricle where fewer major coronary vessels reside, and involves a lower-pressure car-diac area (right ventricle and atrium), which is less likely to bleed profusely if the myocardium is punctured. As such, it is the safer and therefore preferred approach and will be the only one described here.

A. Explain procedure to patient Make sure it is fully under-stood that surgical intervention may be required. Place an in-travenous line and keep it open with a slow drip. Mild seda-tion is helpful.

Technique 201

B. Assemble proper equipment The needle used depends on the nature of the suspected fluid. In general, a 16- or 18-gauge spinal needle that is 8 to 12 cm long is satisfactory. A short, beveled needle should be used to minimize the danger of lac-eration. A number of plastic catheters (PE160 or 190) or nee-dle-catheter kits are available and can be used to decrease the risk of myocardial damage or to be left in place for several days for continuous drainage or intrapericardial drug instil-lation. If a catheter is used, one must be aware that if bent or pulled against the bevel of the needle during insertion, the tip of the catheter may break off inside the pericardium. A sterile extra length of well-insulated wire with alligator clamps at each end will be needed to connect the needle to the chest lead of the electrocardiograph (see Fig 16-1) .

Other equipment needed includes syringes (10 and 50 ml), three-way stopcock, local anesthetic, needles (25- and 21-gauge), sponges, towels, antiseptic solution, mask, gloves, gown, assorted tubes for collecting samples (basin, culture tube, cytology bottle, hematocrit tube), and clamps.

A resuscitation cart, defibrillator, and electrocardiograph, should be in the room.

C. Position patient The patient should be in the sitting or semiupright position. This will cause the xiphoid process to protrude anteriorly and the pericardial fluid to gravitate in-ferolaterally and posteriorly.

D. Attach limb leads of the electrocardiograph Leave the chest or precordial V lead from the machine free and easily acces-sible. The electrocardiograph or oscilloscope should be in clear view of the operator, who should be monitoring it closely to-gether with an assistant.

E. Mark point of entry It is the left xiphosternal angle, 3 to 4 mm below the costal margin (see Fig 16 -1 , inset).

F. Don gloves, wear sterile gown, and use mask.

G. Cleanse a wide area around the point of entry with iodine solution. Drape the field.

H. Deliver anesthetic Infiltrate the point of entry and the path of the needle with local anesthetic. As the anesthetic needle is advanced, check for pericardial fluid by aspirating prior to in-jection.

I. Connect the pericardiocentesis needle by a three-way stop-cock to a 50-ml syringe. Connect one free alligator clamp at the end of the electrical wire to the hub of the needle. The other end is now connected to the chest lead of the electrocar-diograph. This makes the needle into an exploring electrode that, on contact with the myocardium, will show either a cur-

202 Pericardiocentesis

rent of injury (ST-segment elevation on contact with the ven-tricle and PR-segment elevation on touching the atrium) or premature ventricular or atrial contractions. This is best seen in leads II, III, or aVF, although it may be seen in all leads.

It is important that the operator be aware of the limitations of this technique.

1. Electrical disturbances created while the needle is being advanced through the chest wall may have a marked damp-ing effect on the tracing and may therefore result in miss-ing the current of injury.

2. The needle may traverse an electrically silent area in the myocardium (tumor infiltrate, myocardial infarct, storage disease) that will not elicit a current of injury and will re-sult in fatal laceration of the ventricle.

3. Unless the equipment is perfectly grounded, attaching the needle to an electrocardiograph increases the danger of ac-cidental ventricular fibrillation.

J. Insert the needle perpendicular to the skin, at the marked point of entry in the left xiphosternal angle, through a small stab wound; then depress gradually with every 5- to 10-mm advancement until it is at an angle 40 to 45 degrees with the abdominal wall. It is useful to have 2 ml of saline in the sy-ringe to permit flushing of the needle after entry into subcu-taneous tissue in order to clear it of tissue fragments prior to puncture of the pericardium.

The needle should be directed toward the right shoulder. It is suggested by some authors that the needle be directed me-dially or toward the left shoulder. However, that direction will lead the needle closer to the posterior descending coronary ar-tery or other large coronary arteries. The path of the needle will be along the posterior surface of the sternum.

Advance the needle a few millimeters at a time, aspirating intermittently and monitoring the ECG continuously.

The distance from the skin to the pericardium is 6 to 10 cm in an adult and 5 cm or less in a child. During the course of entry one may feel a tough elastic resistance as the diaphragm is penetrated, a distinct "give" or "pop" when the pericardium is punctured, and a definite "ticking" or "grating" sensation transmitted to the fingers when the epicardial surface is con-tacted. Should the latter occur, immediately withdraw the needle a few millimeters and redirect it.

K. Obtain and observe fluid When fluid is obtained, note the color of the initial return. At this point, if only needle aspira-tion is to be done the needle should be stabilized by placing a clamp at the skin surface. If a catheter is to be inserted, re-move the syringe; advance the catheter through the needle;

Technique 203

remove the needle very carefully, making sure that the end of the needle is not encountering any resistance from a kinked catheter, which may result in shearing the free end of the catheter by the beveled end of the needle. If the catheter is to be left in place, secure it to the skin with a suture, apply a broad-spectrum antibiotic ointment at the point of entry, and cover the area with an occlusive dressing.

Removal of as little as 50 ml of fluid will result in relief of cardiac tamponade. However, as much fluid as is possible should be removed to delay rapid reaccumulation. If the fluid is grossly bloody, it is important to know quickly whether the needle has penetrated the heart prior to removal of any fluid. This may be accomplished by one of the following methods:

1. Simultaneous microhematocrit determination of venous blood and pericardiocentesis fluid. As a rule, the hematocrit reading of pericardial fluid is lower than that of venous blood, except in acute hemorrhagic pericarditis.

2. Observe the fluid for clotting. Clotting will occur if blood is obtained from the heart or one of the coronary vessels but will fail to occur with bloody pericardial fluid. In the post-operative anticoagulated patient, this loses its usefulness as a discriminating test.

3. Inject 1 ampule of dehydrocholate (Decholin) sodium through the needle or catheter. If injection is made into the cardiac cavity, the patient will taste it within seconds. In the unconscious or uncooperative patient this test becomes unreliable.

4. Inject indocyanine green dye through the needle or catheter and record its appearance with an earlobe densitometer. This requires specialized cardiac laboratory equipment.

5. Record the pressure of the pericardial catheter and compare it to the central pressures. This requires a previously mon-itored patient with central catheters already in place.

6. Simultaneously determine the pH and Pco2 and Po2 levels of venous blood and pericardial aspirate. Pericardial fluid should be collected in the same careful anaerobic manner as arterial blood. The pericardial fluid has a substantially higher Pco2 level and a lower Po2 level and pH.

L. Failure to obtain fluid Failure of pericardiocentesis to deliver fluid does not rule out pericardial effusion or tamponade. Fluid will be obtained in half the cases where the echocardi-ogram indicates posterior loculation and in over 90% in those cases with a large volume of anteriorly located fluid.

M. Roentgenograms It is useful to inject air or sterile carbon dioxide into the emptied pericardial sac for roentgenographic

204 Pericardiocentesis

diagnostic procedures. The volume injected is half of the vol-ume of fluid removed, up to a maximum of 200 ml. Films taken with the patient in various positions will help delineate heart size, fluid loculation, thickness of the pericardial sac and possible neoplastic infiltrates.

Prior to air injection it is absolutely essential to be sure that the needle or catheter is in the pericardial sac in order to avoid an air embolus. If an air embolus results or is suspected, place the patient on the left side with the head down.

N. Withdraw needle and follow up After the procedure is com-pleted, withdraw the needle or catheter. Apply a sterile dress-ing. Closely monitor the patient for signs of tamponade (in-creasing pulsus paradoxus, hypotension, shortness of breath, cyanosis, rising venous pressure).

IV. COMPLICATIONS

A. Laceration of myocardium or coronary vessel Even in ex-perienced hands and with careful monitoring this is an inher-ent potentially fatal complication. Any time grossly hemor-rhagic fluid is obtained it is important to quickly determine whether the needle has penetrated the heart. Most patients will recover without sequelae but will require very careful and close monitoring for tamponade.

B. Ventricular arrhythmias Irritation of the ventricle on epicar-dial contact is the cause of this complication, which may result in a serious arrhythmia such as ventricular fibrillation, re-quiring immediate therapy to prevent a fatal eventuality. A cardiac resuscitation cart and a defibrillator should always be immediately available. A poorly grounded or isolated electro-cardiograph must be avoided to prevent the risk of inducing' arrhythmias.

C. Vasovagal reactions Hypotension and bradycardia respon-sive to atropine may occur. In the already hemodynamically compromised patient this may further aggravate the clinical condition of the patient, unless it is recognized and treated rapidly.

D. Puncture of lung with resultant pneumothorax Always ob-tain postpericardiocentesis films.

E. Perforation of abdominal viscus, usually stomach It is im-portant to ascertain by physical examination that the patient does not have a distended stomach or paralytic ileus with dis-tended bowels.

F. Air embolism If the needle is in a cardiac chamber when air is injected at the end of the procedure, an air embolism

Interpretation 205

with its dramatic and serious consequences will occur. Imme-diately place the patient on the left side and lower the head of the bed.

V. INTERPRETATION Fluid obtained on pericardiocentesis should be submitted for blood cell count and differential cell count; he-matocrit reading; protein determination; and cytologic examina-tion and culture. Further tests may be obtained as indicated be-low, depending on the diagnosis under consideration. A Gram stain should be done on the fluid and examined either by the physician performing the procedure or by an assistant immedi-ately on completion of the tap. It has been estimated that a spe-cific diagnosis can be made from fluid examination alone in 25% of the cases and a new, previously unsuspected diagnosis made in 7% of the cases.

If it is determined that the bloody fluid is not due to blood as-pirated from a cardiac or vascular cavity, the most likely possi-bility will be a neoplastic effusion or at times tuberculosis or uremic pericarditis.

Effusion due to neoplasms will yield abnormal cytologic find-ings in as many as 87% of cases. The yield from pericardial bi-opsy examination appears to be lower, but experience in this is limited.

Tuberculous pericarditis will very rarely be diagnosed on acid-fast stain of the fluid obtained, but nevertheless acid-fast stain should be performed. Cultures will be negative in 40% to 60% of the cases in which cultures are obtained. Pathologic examination of pericardial tissue offers the best results, with a diagnostic yield of 87% to 100%. As with most other tuberculous effusions, the pericardial fluid will have a high protein content (>3 gm/dl), the cellular content will be mostly lymphocytic, and if a lactic dehy-drogenase level is obtained it will be elevated.

The most important diagnosis to rule out is acute bacterial pericarditis. The fluid will be purulent, with a predominance of polymorphonuclear leukocytes; the protein content will be ele-vated and organisms will be identified on Gram stain and cul-ture. In general, there will be associated evidence of infection with leukocytosis, fever, and an identifiable source of infection.

The pericardial effusion of rheumatoid arthritis will have a low glucose and complement content but a high lactic dehydrogenase and -y-globulin level, with a positive rheumatoid factor test.

The fluid in congestive heart failure will have the features of a classic transudative effusion.

The fluid of a posttraumatic pericarditis due to myocardial lac-eration will be hemorrhagic. The fluid will be grossly bloody from the outset rather than turning bloody, as with taps due to trau-matic laceration during the procedure itself.

206 Pericardiocentesis

REFERENCES Shabetai R.: The pericardium: An essay on some recent develop-ments. Am. J. Cardiol. 42:1036-1043, 1978.

A review of recent developments in our knowledge of the normal and abnormal pericardium.

Shabetai R. (ed.): Pericardial disease. Am. J. Cardiol. 26:445-489 1970.

A broad but selective review of pericardial disease covering its med-ical history, functional significance, anatomy, differential diag-nosis, and the dynamics of pericardial effusion.

Agner R.C., Gallis H.A.: Pericarditis: Differential diagnostic consid-erations. Arch. Intern. Med. 139:407-412, 1979.

A good article. In 90% of 133 cases analyzed retrospectively, initial assessment, without pericardiocentesis, provided a correct diagno-sis. Certain initial diagnoses (idiopathic, uremic, rheumatologic) seemed at greater risk of error than others (tuberculous, neoplas-tic). Underlying tuberculous or malignant pericarditis were the most common sources of error on initial assessment.

Spodick D.H.: Differential diagnosis of acute pericarditis. Prog. Car-diovasc. Dis. 14:192-209, 1971.

A good review. Spodick D.H.: Acute cardiac tamponade: Pathologic physiology, di-agnosis and management. Prog. Cardiovasc. Dis. 10:64-96, 1967.

An excellent review. Though parts of this article are outdated, it still provides one of the most comprehensive and clinically practical discussions of the topic.

Kotte J.H., McGuire J.: Pericardial paracentesis. Mod. Concepts Cardiovasc. Dis. 20:102-103, 1951.

A summary statement on the state of the art in 1951. Krikorian J.G., Hancock E.W.: Pericardiocentesis. Am. J. Med. 65:808-814, 1978.

A review of the experience with pericardiocentesis in 123 patients. Bishop L.H., Estes E.H., Mcintosh H.D.: The electrocardiogram as a safeguard in pericardiocentesis. J.A.M.A. 162:264-265, 1956.

The pericardiocentesis needle, connected to an ECG set to record chest leads, constitutes an exploring electrode that, on contact with the myocardium, will detect an injury current if the needle contacts the ventricular (ST-segment elevation) or atrial (PR-segment ele-vation) epicardium.

Sobol S.M., Thomas H.M., Evans R.W.: Myocardial laceration not demonstrated by continuous electrocardiographic monitoring occur-ring during pericardiocentesis. N. Engl. J. Med. 292:1222-1223, 1975.

A discussion of myocardial laceration due to needle entry through metastatic tumor, which, being electrically silent and incapable of generating an injury current, escaped ECG detection.

Stone J.R., Martin R.H.: Bloody pericardial fluid or intracardiac

References 207

blood? A method for quick and accurate differentiation. Ann. Intern. Med. 77:592-594, 1972.

Indocyanine green dye is injected through the pericardiocentesis needle and its appearance time is measured by earlobe densitome-try: a procedure reserved for the appropriately equipped cardiac laboratory.

Mann W., Millen J.E., Glauser F.L.: Bloody pericardial fluid: The value of blood gas measurements. J.A.M.A. 239:2151-2152, 1978.

Compared to simultaneously determined blood gas values, hemor-rhagic pericardial fluid has a substantial increase in Pco2 levels and a decrease in Po2, pH, and bicarbonate levels.

Balakirshnan S., Hartman C.W., Grinnan G.L.B., et al.: Pericardial fluid gas analysis in hemorrhagic pericardial tamponade. Ann. Thorac. Surg. 27:55-58, 1978.

Further evidence that the simultaneous measurement of Po2 and Pco2 levels of central venous blood and pericardial fluid is a useful, rapid bedside method to confirm the site of hemorrhagic aspirate during pericardiocentesis. Pericardial fluid has a significantly higher Pco2 level and a lower Po2 level.

Santos G.H., Frater R.W.M.: The subxiphoid approach in the treat-ment of pericardial effusion. Ann. Thorac. Surg. 23:467-470, 1977.

An argument in favor of subxiphoid pericardiotomy for the diag-nosis (tissue obtained) and treatment (lower rate of recurrence) of nontraumatic pericardial effusion.

Smith F.E., Lane M., Hudgins P.T.: Conservative management of malignant pericardial effusion. Cancer 33:47-57, 1974.

A review of the medical literature and the authors' experience with five cases on the value of local instillation of alkylating agents in the treatment of malignant pericardial effusions.

Davis S., Sharma S.M., Blumberg E.D., et al.: Intrapericardial tet-racycline for the management of cardiac tamponade secondary to malignant pericardial effusion. N. Engl. J. Med. 299:1113-1114, 1978.

The technique was successfully used in six cases. Martini N., Freiman A.H., Watson R.C., et al.: Intrapericardial in-stillation of radioactive chromic phosphate in malignant pericardial effusion. A.J.R. 128:639-641, 1977.

Another mode of therapy for malignant pericardial effusion. Buselmeier T.J., Simmons R.L., Najarian J.S., et al.: Uremic pericar-dial effusion: Treatment by catheter drainage and local nonabsorb-able steroid administration. Nephron 16:371-380, 1976.

The technique is described and its successful use in 11 of 12 pa-tients is reported. The pericardial fluid is drained through an in-dwelling catheter and 100 mg of triamcinolone hexacetonide is in-stilled. A 35-ml syringe with a three-way stopcock is connected to the catheter and is used for repeated drainage and steroid admin-istration at 4- to 6-hour intervals until no further drainage is ob-tained.

18 Cardioversion

I. INDICATIONS Direct current precordial shock is used to termi-nate supraventricular or ventricular tachyarrhythmias. Its indi-cations are the emergency treatment of acute tachyarrhythmias and the elective cardioversion of chronic atrial fibrillation or flutter.

A. Emergency cardioversion

1. Supraventricular arrhythmias

a. Atrial or junctional tachycardia not responding to drugs or vagal maneuvers and/or associated with hemody-namic deterioration.

b. Atrial flutter or fibrillation resulting in major hemody-namic disturbances in patients with acute myocardial infarction.

c. Drug-resistant tachyarrhythmia in patients with Wolff-Parkinson-White syndrome.

2. Ventricular arrhythmias

a. Ventricular fibrillation.

b. Ventricular tachycardia, unresponsive to lidocaine therapy, in patients with acute myocardial infarction.

C. Nonparoxysmal ventricular tachycardia in patients who are hypotensive and in whom the arrhythmia is not ter-minated by speeding up the S-A node rate with atro-pine.

B. Elective cardioversion

1. Cardioversion should be considered in the following sit-uations:

a. Atrial flutter. Cardioversion is the treatment of choice for atrial flutter because of the good responsiveness of this arrhythmia.

208

Complications 209

b. Atrial fibrillation of less than one year's duration. Oth-erwise digitalis is the drug of choice, unless there is an associated hemodynamic impairment. In general the longer the duration of atrial fibrillation the lower the success rate of cardioversion and the greater the rate of reversion to the original rhythm disturbance.

c. Recent onset of atrial fibrillation/flutter or that persist-ing postoperatively after surgical correction of a hemo-dynamic abnormality.

d. Persistent atrial fibrillation in thyrotoxic patients, after they have been rendered euthyroid.

e. Atrial fibrillation associated with embolic episodes in the past.

f. Reversion to atrial fibrillation after 3 to 6 months of sinus rhythm following initial cardioversion should be considered for repeated cardioversion.

g. Paroxysmal atrial tachycardia or nodal tachycardia re-fractory to other forms of therapy.

2. Cardioversion may be considered but should be delayed in the following situations:

a. Untreated hyperthyroidism associated with atrial fi-brillation.

b. Atrial fibrillation and recent embolic episodes.

C. Patients with atrial fibrillation about to undergo car-diac surgery for repair of mitral valve disease.

d. Patients with hypokalemia in addition to atrial fibril-lation.

3. Cardioversion may be considered but is unlikely to be beneficial in the following situations:

a. Massive cardiomegaly and congestive heart failure.

b. Elderly patients with asymptomatic atrial fibrillation.

C. Atrial fibrillation associated with marked left atrial en-largement.

4. Cardioversion is indicated but countershock may be dangerous; consider conversion by rapid atrial pacing in the following situations:

a. Tachyarrhythmias due to digitalis intoxication.

b. Tachyarrhythmias during sick sinus syndrome where long sinus arrests have been noted.

210 Cardioversion

II. CONTRAINDICATIONS

A. Digitalis toxicity. Direct current shock is not only ineffective in converting digitalis-induced arrhythmias, but also, because of the digitalis-induced lowered fibrillatory threshold, it may induce a potentially fatal ventricular arrhythmia.

B. Atrial fibrillation or flutter associated with complete heart block.

C. Atrial fibrillation associated with slow ventricular response without digitalis therapy, particularly in the elderly asymp-tomatic patient.

D. Hypokalemia and atrial fibrillation.

E. Atrial flutter or fibrillation in association with hypoxia, hy-percapnia, acidosis, or alkalosis.

F. Atrial fibrillation of more than 2 months' duration in associa-tion with mitral stenosis or insufficiency.

G. Recurrent disturbances of atrial rhythm in rapid succession.

III. TECHNIQUE

A. Precardioversion preparation Cardioversion is best done in a well-monitored and carefully controlled environment, such as the coronary care unit, with physicians experienced in the treatment of cardiac arrhythmias in attendance. Equipment for complete cardiopulmonary resuscitation must be at the bedside.

1. Explain procedure to patient Also obtain a signed in-formed consent at this time. Avoid terms such as "electric shock" or "stopping the heart." Use reassuring words such as "current" or "changing the rhythm of the heart to normal."

2. Prepare patient In elective procedures, the patient should be fasting for about 8 hours before the procedure. In an anxious patient, a short-acting parenteral sedative may be given 1 hour before the procedure. All dentures should be removed. In emergency procedures, establish ad-equate airway patency and good oxygenation before un-dertaking electroshock.

3. Atropine Any patient receiving a (3-blocker, any patient in whom atrial fibrillation has been present for over 3 to 5 years, and any patient with atrial fibrillation and a ven-tricular response rate of 70 beats per minute or less should be given 1 to 2 mg of atropine intravenously to protect against serious bradycardia or asystole immediately after shock.

Technique 211

4. Quinidine need not be discontinued. Although debated, there is no good evidence that the routine prophylactic use of quinidine or of other antiarrhythmic drugs before the procedure is beneficial.

5. Anticoagulation Patients with long-standing atrial ar-rhythmias or with a history of embolic episodes should be well anticoagulated with an oral anticoagulant for at least 2 weeks before elective cardioversion. Use intravenous heparin when the need for cardioversion is urgent.

6. Correction of electrolyte imbalances Electrolyte imbal-ances, in general, but hypokalemia, in particular, must be corrected prior to undertaking electroconversion.

7. Intravenous infusion Start an intravenous infusion to provide access to the circulation should the need arise to administer intravenous medications during the procedure.

8. ECG and blood pressure Place complete ECG monitor leads and a blood pressure cuff.

9. Position of patient The patient should be supine, with a board under the back to facilitate cardiopulmonary resus-citation should it become necessary. The patient must not be touching any metal portion of the bed, as otherwise se-rious burns may occur. Disconnect and remove all other electrical equipment.

B. Cardioversion procedure

1. Record baseline vital signs.

2. Obtain complete 12-lead ECG.

3. Determine which ECG lead exhibits best complexes. Tall QRS complexes and a good P wave are desired. Set the synchronized cardioverter on that lead. The cardio-verter is equipped with a time delay circuit triggered by the R wave of the ECG such that the shock is timed to be delivered approximately 10 msec after the peak of the R wave and on its downslope, thereby avoiding the vulnera-ble phase in late systole when the ventricle is susceptible to fibrillation. When S waves are prominent in limb leads, these may be used as the triggering complexes by revers-ing the polarity on the oscilloscope screen.

4. Test the synchronization of the cardioverter by holding the paddles together, discharging the machine, and noting where a "spike" appears. It should occur precisely in the QRS complex, on the downslope of the R wave.

5. Set machine to desired energy level (Table 18-1) . Compli-cations of cardioversion are higher with higher energy set-tings and small energy levels should be used at first. If

212 Cardioversion

T a b l e 1 8 - 1 CARDIOVERSION: R E S U L T S A N D E N E R G Y S E T T I N G S

these are unsuccessful, higher levels may be tried. For an adult, an initial sett ing of 25 joules is usual ly satisfactory, although atrial flutter will frequently convert at 10 joules. Exceptions to this are as follows:

a. In digitalized patients start at 5 joules, followed by in-crements of 5 to 10 joules to 10, 25, 50, 100, 200, 300, if

b. The initial sett ing for ventricular fibrillation, with no synchronizer in circuit, should be 400 joules.

C. Patients with severe ischemic heart disease or cardio-myopathy require higher energy levels for cardiover-sion and also will have a greater incidence of serious complications.

6. Inject slowly 5 to 10 mg of diazepam (Valium) intrave-nously to provide amnesia and sedation. Anxious individ-uals may require 15 to 20 mg of diazepam. They, however, do not convert as easily. Following injection, ask the pa-tient to count backward from 100 until the count becomes garbled, erratic, and repetitive (usually at 60 to 50). At this time the patient will be conscious but somnolent and ready to be shocked.

7. Recheck vital signs after patient is asleep.

8. Reduce skin resistance, establish good electrical contact, and prevent skin burns. Either:

a. Apply a thick, even layer of conductive electrode jelly to the paddles, or

b. Apply saline pads to the chest wall. Alcohol-soaked pads should not be used because they may catch fire.

needed.

EXPECTED ELECTRICAL SUCCESSFUL ENERGY SETTING

DYSRHYTHMIA ELECTROVERSION (9,) IW-SEC)

Atrial fibrillation Organic heart disease 85-90 50-250 in >70% Idiopathic <75 Higher in <30%

Atrial flutter 90-95 20-100 Paroxysmal atrial 75-80 20-100

tachycardia Ventricular tachycardia 97 25-100 (up to

400 in some) Ventricular fibrillation 60 400

Technique 213

Hirsute patients should have an appropriately sized area shaved for good paddle contact.

9. Apply paddles firmly to chest. Make sure they are not in direct contact with skin. Too firm an application of the paddles results in bridging of current and skin burns. Pad-dle placement may be:

a. Anterior-posterior. One paddle is placed anteriorly over the second and third intercostal space just below and lateral to the sternomanubrial line; the other, flat pad-dle, is placed posteriorly just below and between the tip of the left scapula and the vertebral column. The pa-tient lies on the flat paddle, and it is only the anterior paddle that needs to be held by the operator.

b. Anterior. One paddle is over the base of the heart, be-low the right clavicle lateral to the sternal border; the other is over the apex of the left heart, lateral to the left nipple in the fifth intercostal space along the ante-rior axillary line.

10. Stand back from bed. Order all other personnel away from the bed. Make sure the patient has not come in contact with the bed and that all other electrical equipment has been removed.

11. Administer shock. The shock will result in transient arousal of the patient, muscular contraction of the upper extremities, and a brief outcry. A brief period of sinus ar-rest followed by bradycardia or sinus arrhythmia fre-quently occurs 1 to 2 seconds after the procedure before restoration of sinus rhythm. Failure of this to correct after a few minutes may indicate "sick sinus syndrome."

a. If sinus rhythm is not established at the initial voltage setting, increase the energy setting in increments to 50, 100, 200, 300, or 400 joules, with pauses between at-tempts to assess the ECG rhythm.

b. Should sinus rhythm fail to emerge and ventricular ex-trasystoles occur after a shock, inject 50 mg of lidocaine through the intravenous line. When the ectopic beats are controlled, repeat the shock at the same setting.

c. If after a shock normal sinus rhythm occurs briefly, only to convert spontaneously back to the original ar-rhythmia, then chances of converting the patient are minimal and cardioversion may best be abandoned in favor of drug therapy.

d. Should ventricular fibrillation occur as a complication

214 Cardioversion

of the shock, place the machine immediately on the de-fibrillation mode—synchronizer circuit off—set it at 400 joules, recharge it, and administer another shock.

C. Postcardioversion care

1. Record blood pressure and vital signs at half-hour inter-vals. Continue this until values are stable and at pretreat-ment level.

2. Obtain 12-lead ECG and rhythm strip.

3. Monitor patient for at least 12 to 24 hours.

4. Most reversions to the arrhythmia occur in the first month after cardioversion, with the highest incidence of these oc-curring within the first 24 hours. In general the patients who are difficult to convert to sinus rhythm are the ones who are also difficult to maintain in sinus rhythm.

5. Depending on the individual patient, consider long-term maintenance antiarrhythmic and anticoagulant therapy.

IV. COMPLICATIONS As a rule, complication rates are proportional to the energy levels used. The incidence is about 5% at an energy level setting of 150 joules, increasing to about 25% to 30% at 400 joules.

A. Ventricular fibrillation or tachycardia Occasionally, due to improper synchronization, this is more commonly encountered in patients with digitalis toxicity or electrolyte imbalance, es-pecially hypokalemia.

B. Dislodgment of intracardiac thrombi with peripheral emboli-zation occurs in 1% to 3%. The risk is higher in patients with. recent myocardial infarction, chronic ischemic heart disease, mitral valve disease, cardiomyopathy, prosthetic heart valves, or a previous history of embolization. All such patients should be anticoagulated prior to shocking.

C. An increase in cardiac size and pulmonary edema occurs in 3% of patients within 1 to 3 hours of conversion to normal sinus rhythm. The mechanism is unknown but it has been postulated to be due to atrial paralysis. Patients should be monitored closely for the development of this eventuality and treated appropriately for the pulmonary edema.

D. Elevated muscle enzyme levels, most often serum glutamic oxaloacetic transaminase and creatine phosphokinase, are ob-served in 10% of patients. This is due to skeletal muscle dam-age, usually following high-energy countershock, and it is of no clinical consequence.

E. Hypotension develops in 3% of cases, especially after the use

References 215

of higher voltages. It is not related to the anesthetic used. It may persist for several hours and requires careful patient monitoring and appropriate supportive therapy.

F. Electrocardiographic changes in myocardial injury may be observed in 3% of cases, commonly with high energy settings. It may persist for several months.

G. The injection of diazepam may result in transient hypoten-sion. Inject the drug slowly, check the blood pressure after its injection, use no more than 20 mg, and postpone electroshock until the pressure returns to normal.

H. Transient rhythm disturbances occur after shock administra-tion and are of no clinical importance. If ventricular prema-ture contractions occur following shock, give 50 to 100 mg of lidocaine intravenously.

I. Superficial skin burns will occur if jelly is applied poorly and the paddle comes in contact with skin.

J. Vague chest discomfort is a common complaint in some pa-tients, especially after shock at high energy settings.

K. Electrical shock to the operator or to the assistants is the un-fortunate consequence of poor technique and negligence on the part of the operator.

REFERENCES

Lown B., Amarasingham R., Neuman J.: New method for terminat-ing cardiac arrhythmias: Use of synchronized capacitor discharge. J.A.M.A. 182:548-555, 1962.

The original article on the use of dc countershock in the treatment of cardiac arrhythmias.

Chung E.K.: Use and abuse of direct current shock. Cardiology 55:310-320, 1970.

A good review of indications, contraindications, and complications of cardioversion.

Resnekov L.: Present status of electroversion in the management of cardiac dysrhythmias. Circulation 47:1356-1363, 1973.

A review of the theoretical and practical considerations of electrical reversion of cardiac dysrhythmias.

Resnekov L.: Theory and practice of electroversion of cardiac dys-rhythmias. Med. Clin. North Am. 60:325-342, 1976.

A summary of the theory, "do's" and "dont's," technique, and re-sults of electroconversion.

Resnekov L.: Drug therapy before and after the electroversion of car-diac dysrhythmias. Prog. Cardiovasc. Dis. 16:531-538, 1974.

A summary statement on the appropriate use of drugs with electri-cal therapy to maintain the patient in sinus rhythm.

216 Cardioversion

Peters R.W., Scheinman M.M.: Emergency treatment of supraven-tricular tachycardia. Med. Clin. North Am. 63:73-92, 1979.

A brief review of the diagnosis, mechanism, clinical picture, and therapy of supraventricular tachycardias.

Resnekov L., McDonald L.: Complications in 220 patients with car-diac dysrhythmias treated by phased direct-current shock and indi-cation for electroversion. Br. Heart J. 32:600, 1970.

In this study of220 patients, complications followed in 14.5% and were related to higher energy settings, especially those exceeding 300 joules.

19 Temporary Ventricular

Pacing

Cardiac pacing is a complex discipline requiring extensive knowl-edge and experience in cardiology, electrophysiology, and pacemaker component electronics. Many rhythms and conduction abnormalities, including preexcitation syndromes, atrial tachycardias, sick sinus syndrome, and various bradyarrhythmias and ventricular arrhyth-mias, may benefit from cardiac pacing; however, therapy with phar-macologic agents will often suffice until expert opinion regarding the advisability of artificial pacing becomes available. This section will be limited in content to temporary ventricular pacing, since this is the only commonly needed form of pacing that a house officer may be expected to perform on an emergency basis. Transvenous ventric-ular pacing, temporary external cardiac pacing, and temporary transthoracic cardiac pacing are discussed; all other forms of pacing (e.g., permanent ventricular pacing, atrial pacing) should be per-formed and managed by a cardiologist experienced in all aspects of cardiac pacing and its complications.

I. INDICATIONS Temporary ventricular pacing has its major util-ity in the emergency control of life-threatening arrhythmias or their precursors and should be maintained until they resolve spontaneously, respond to medical treatment, or until permanent pacing is instituted. For practical purposes the indications for emergency temporary ventricular pacing are cardiac standstill and symptomatic heart block affecting cardiac output and perfor-mance. This will usually be either in patients with acute myocar-dial inferior or anterolateral infarction or in patients with degen-erative disease of the fascicular conduction system. Symptoms that constitute an indication for pacing are Stokes-Adams attacks characterized by dizziness or syncope due to cerebral ischemia, progressive manifestation of intractable heart failure, hypoten-sion with inadequate peripheral tissue perfusion, and accelerated anginal symptoms.

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218 Temporary Ventricular Pacing

A. Incomplete heart block

1. First-degree atrioventricular block

a. ECG P-R interval of more than 0.20 seconds without other conduction defects.

b. Causes Usually caused by a conduction delay be-tween the SA node and the atrioventricular (AV) node between the AV node and the bundle of His, or within the AV node itself.

C. Cardiac injury or drugs such as quinidine, digitalis, or propranolol may produce this defect. It may occur in the absence of heart disease or exposure to pharmacologic agents.

d. Treatment. If not symptomatic, it does not require pacing.

2. Second-degree atrioventricular block

MOBITZ TYPE I AV BLOCK or Wenckebach block

a. ECG Progressive prolongation of the P-R and short-ening of the R-R interval until a QRS complex is dropped, in a cyclic fashion. A paradoxical Wenckebach block refers to the variability of the P-R interval of shortening and lengthening sequence followed by a dropped QRS complex.

b. Causes The conduction defect is in the AV node. It is commonly due to acute inferior myocardial infarction or digitalis toxicity.

c. Treatment Usually transient and asymptomatic. It does not require pacing in the majority of cases.

MOBITZ TYPE II AV BLOCK

a. ECG Normal P-R interval with abrupt absence of QRS complexes after normally occurring P waves.

b. Causes The conduction block is in the bundle of His or below.

c. Treatment The appearance of this abnormality in an acute setting is ominous and will often progress to com-plete heart block in short order. The majority of these patients—as many as 85%—are symptomatic and will require pacing. If time permits, seek the advice and as-sistance of an experienced cardiologist as soon as the defect is identified.

Complications 219

B. Complete heart block

1. Third-degree heart block

a. ECG Complete atrioventricular dissociation with in-dependent atrial and ventricular pacemakers. An ECG entity known as isorhythmic dissociation can easily be confused with AV block and dissociation. Isorhythmic dissociation refers to the speeding up of the function pacemaker over the atrial pacemaker. This entity, then, represents an electrophysiologic block and not a true AV block. The escape rhythm of third-degree block may be as follows:

(1) Junctional with normal QRS complexes of less than 0.12 seconds. Digitalis toxicity must be entertained as the possible cause of the AV dissociation. Ventric-ular pacing in this situation is hazardous and may induce a fatal ventricular arrhythmia. Withdrawal of digitalis is often all that is required. Potassium supplementation in this setting may aggravate the situation rather than improve it. If marked potas-sium depletion is present, potassium should be re-placed cautiously.

Narrow QRS complexes are also encountered in is-chemic heart disease and in congenital heart block. For these, obtain expert opinion to determine the possible benefits of pacing.

(2) Idioventricular with wide QRS complexes of more than 0.12 seconds, occurring at a rate of 30 to 40 per minute. The block is at or below the bundle of His. Most of these patients are symptomatic and will re-quire permanent pacing after stabilization with temporary ventricular pacing.

The development of right bundle-branch block (RBBB) by itself or with either left anterior hemiblock (LAHB) or left posterior hemiblock (LPHB) in the course of ischemic heart disease as an indication for ventricular pacing is a difficult problem. Opinions vary greatly concerning pacing in bifasci-cular block and will require expert advice in its management. Chronic RBBB with LAHB or LPHB is often not paced unless it produces symptoms. On the other hand, with the combina-tion of RBBB and LAHB or LPHB developing in a patient with acute myocardial infarction, most authorities proceed with temporary pacing since 20% to 60% of patients develop complete heart block. Even with pacing, the prognosis is poor and is more closely related to the degree of myocardial injury than to the conduction defect. However, with recovery from the injury, this is a transient complication and pacing can be

220 Temporary Ventricular Pacing

withheld unless the patient is symptomatic or there is associ-ated first-degree heart block.

C. Cardiac standstill Complete absence of electrical activity is usually encountered during cardiopulmonary resuscitation. If electrical activity cannot be reestablished with precordial thumping or with pharmacologic agents, emergency ventricu-lar pacing is the only means remaining that could possibly initiate the patient's own electromechanical cardiac function. The state of myocardial function is usually quite poor in this setting, and it is probably for this reason that even ventricular pacing will often prove to be ineffectual.

In summary, the four most important questions to consider in determining the need for emergency cardiac pacing are as fol-lows:

1. Is the patient symptomatic because of his conduction prob-lem?

2. Is there any hemodynamic impairment as a result of conduc-tion difficulty?

3. If the conduction problem is second-degree heart block, is it type I or type II?

4. If AV dissociation is present, are the QRS complexes wide or narrow?

II. CONTRAINDICATIONS

A. Nonemergency situations

B. Conduction abnormalities or arrhythmias not related to symptomatic heart block or cardiac standstill

C. Inexperience

D. Uncertainty about ECG interpretation

E. Anticoagulants should be discontinued prior to pacing and never used after transvenous wire insertion.

III. TECHNIQUE

A. Temporary transvenous pacing

1. Environment Ventricular pacing is best done in a well-monitored and controlled environment (catheterization laboratory or coronary care unit) with experienced physi-cians in attendance. In emergency situations, it may be done at the bedside. Under all circumstances, complete re-suscitative equipment must be available at the bedside. Proper grounding of all equipment must be strictly ob-served.

Technique 221

2. Explain the procedure to the patient and/or family and obtain informed consent. Use reassuring terms.

3. Select site of catheter insertion The catheter may be placed either percutaneously or by venous cutdown. It may be introduced at any one of the following venous sites, the technique for each of which has been described previously (see chapter 15):

a. Internal or external jugular vein This site offers the advantages of quick access, excellent alignment with the right atrium, and no tampering with vessels that may need to be utilized for subsequent permanent transvenous pacemaker placement. The disadvantage is esthetic and psychological ("neck cutting").

b. Subclavian vein Same advantages as above.

c. Basilic vein This site is chosen by many operators be-cause of familiarity. Its disadvantages are difficulty in negotiating past the region of the axilla, a higher inci-dence of thrombophlebitis, permanent loss of the vein if a cutdown is used, and, probably most important, in-stability of pacing and greater incidence of complica-tions because of pacemaker wire displacement and mi-gration with movement of the upper extremity after in-sertion.

d. Femoral vein The disadvantage of this route is con-tamination with urine and feces, which, in addition to causing infection, may result in short-circuiting within the external pulse generator. Its advantage is that cath-eter insertion can be accomplished without patient ma-nipulation. In the final analysis, the choice must depend on the per-

sonal experience of the operator and familiarity with can-nulating the vein selected. Use the vein with which you are most familiar.

4. Select pacemaker wire catheter system Most transve-nous pacemaker catheters are either fixed-position "straight" wires or balloon-tipped "floating" wires. The former is best guided to the right ventricle under fluoros-copy, whereas the latter may be placed by ECG or by flu-oroscopic technique. The pacemaker equipment available at each institution varies. The operator must be thor-oughly familiar with the specific pacemaker before pro-ceeding with wire placement.

The catheter terminals should be handled carefully and never touched with bare hands. Use gloves. The terminals should not be in contact with conductive material such as liquid. If they are not connected to the pacemaker, insu-

222 Temporary Ventricular Pacing

late them with a finger rubber glove and fix them to the skin.

5. Use sterile technique Catheter insertion must be done under strict sterile technique. Use masks, gown, and gloves. Cleanse the site of entry and drape appropriately.

6. Insert catheter Venous entry is usually performed with an around-the-needle flexible cannula that is left in the lumen of the vein after the central needle is removed. The internal diameter of the flexible cannula should be large enough to accommodate the pacing catheter. Insert the catheter into the vein through the cannula, which is then withdrawn over the catheter. If the transbrachial entry site cannot be successfully cannulated percutaneously, a venous cutdown may be performed at the cost of sacrific-ing the basilic vein.

7. Position catheter The catheter can be positioned within the trabeculae of the right ventricle either under direct vision using image intensification fluoroscopy or blindly under ECG control.

a. Fluoroscopic method This is the preferred and better method of positioning the catheter. However, when the need arises for rapidly establishing ventricular pacing it may be difficult to move a critically ill patient to a fluoroscopy room, and the portable image intensifier is too expensive and may be unavailable in most institu-tions. Consequently one must be prepared to proceed with the ECG method. The success of achieving pacing under ECG monitoring is about 80%, depending on the skill of the operator. A 30- to 45-minute time limit must be set from the beginning of this bedside procedure to the achievement of ventricular pacing. When, this limit is exceeded, move the patient to a fluoroscopy room and have the catheter placed under direct vision.

In the fluoroscopic method, the catheter is advanced into the pulmonary artery, then withdrawn into the apex of the right ventricle and wedged into the tra-beculae, where the stability of the catheter is optimal. The catheter tip should be anterior and inferior on fluo-roscopy.

b. ECG method (Fig 19-1) The patient is attached to a high-impedance, battery-powered ECG. Careful atten-tion to detail is essential to prevent iatrogenic ventric-ular arrhythmias due to electrical leaks. If 60-cycle in-terference is seen on the ECG tracing, stop the proce-dure until all sources of electrical leaks are investi-gated, found, and corrected. Use care to prevent

Technique 223

Left ^ —-subclavian *—

Fig 19-1.—Electrocardiographic tracings obtained during ad-vancement of catheter for temporary transvenous ventricular pacing.

transmission of current leaks from electrical beds or other electrically powered equipment in use. This oc-curs when the patient's bare skin is in contact with the electrode catheter and the electrical equipment in which there is a current leak. All personnel touching the pacing equipment should wear rubber gloves.

Some knowledge of the contour of the intracardiac ECG is essential in placement of the catheter by this method (see Fig 19-1) . In this technique, the four ECG limb leads are attached to the patient in standard fash-

224 Temporary Ventricular Pacing

ion while the precordial unipolar V lead is attached to the distal tip electrode terminal of the balloon-tipped bipolar pacemaker wire. While monitoring the V lead from the tip of the pacemaker wire on the battery-pow-ered ECG, advance the wire at 4- to 6-cm increments. Inflate the balloon with air while it is in the superior vena cava or high atrium and allow it to "float" into the right ventricle; then withdraw the air.

While in the superior vena cava, the recordings will be similar to tracings from the aVH lead of the ECG. Now advance the catheter a few centimers to the high right atrium and the recordings will show a large neg-ative P wave. As the catheter passes from the right to low right atrial positions, the large negative P wave will change configuration to a biphasic form. As the wire tip crosses the tricuspid valve, the large P wave will diminish in amplitude and a large rS complex of 5 to 15 mV will be seen; the right ventricle has now been entered. At this point, it may be necessary to decrease the standardization of the ECG machine to one-half to one-fourth scale to record the large ventricular com-plexes. If the pulmonary artery is entered, the rS com-plexes will diminish in amplitude and the catheter must be withdrawn slightly and then advanced again until the ventricular rS configuration is obtained.

Then deflate the balloon and advance the wire slowly until the right ventricular endocardium is engaged, as recognized by the appearance of a current of injury (ST elevation) following the rS complex.

8. Attach generator With the pacemaker wire lodged within the trabeculae of the right ventricle, attach the ex-ternal pulse generator in the "power off" position so that the anode ( - ) is connected to the tip or distal electrode terminal of the pacemaker wire and the cathode ( + ) is connected to the proximal electrode terminal of the pace-maker wire for bipolar pacing.

The generator can now be turned on. In most instances, the pulse generator is placed in the synchronous "demand" mode by turning the appropriate switch on the control panel. In cardiac standstill, the asynchronous or fixed rate mode is chosen. The rate is usually set at 70 to 75 beats per minute, but this depends on the clinical situation. As-sess the adequacy of perfusion by feeling the peripheral pulses after paced beats.

9. Adequacy of procedure Successful ventricular pacing now depends on the adequacy of the wire placement, the pacemaker's sensing mechanism, the pacemaker's captur-

Technique 225

ing mechanism, and demand function. The adequacy of each component can be assessed as follows:

a. Adequate wire placement (1) In the unipolar V lead recording, the P wave is de-

creased in amplitude, and a large rS complex fol-lowed by a current of injury is present.

(2) Correct wire tip placement into the right ventricle is confirmed by frontal and lateral chest films, which must be obtained immediately on completion of the procedure.

(3) When the pulse generator is turned on and begins to pace, the surface ECG shows an LBBB pattern to the paced beats. If an RBBB pattern exists, the po-sition is incorrect.

(4) Intact pacing and sensing after deep respiration, coughing, or Valsalva's maneuver is maintained.

b. Adequate sensing

(1) Adequate sensing is usually ensured if the proximal to distal bipolar wire recording QRS amplitude is at least 2 to 3 mV in amplitude. This recording (similar to lead I) is easily obtained by connecting the wire tip or distal electrode terminal to the left arm ECG lead and by connecting the proximal wire terminal to the right arm ECG lead. Lead I is then recorded on the ECG machine.

(2) When the wire terminals are connected to the pulse generator, the appropriate needle on "the control panel will deflect with each of the patient's own ven-tricular complexes, confirming adequate pacemaker sensing function.

c. Adequate capturing

(1) Capturing function is usually ensured if the thresh-old potential is less than 1 mamp, and if the surface ECG shows an LBBB pattern of the captured paced beats.

(2) If the threshold potential is more than 2 mamp, re-position the pacemaker wire for better contact.

(3) If an RBBB pattern to the paced beats is seen on the surface ECG, possibilities include coronary sinus pacing, upper septal pacing, or perforation of the right ventricle. The latter should be suspected when there is transition from an LBBB pattern. An RBBB

226 Temporary Ventricular Pacing

pattern may on occasion be physiologic when the septal Purkinje system depolarizes the left ventricle earlier than the right ventricle.

(4) High threshold potentials may be caused by sleep, a heavy meal, antiarrhythmic agents, and potassium imbalance.

i (5) Low threshold potentials may be caused by exercise and steroids.

d. Adequate demand function This function is easily checked by decreasing the rate of pacemaker discharge to less than the patient's own intrinsic ventricular pace-maker, such that the pulse generator senses the pa-tient's intrinsic discharges and does not discharge on its own.

With the above criteria fulfilled, set the pulse generator output at two to three times the threshold current and at a pacing rate to ensure a normal blood pressure and nor-mal organ perfusion. Remember that high rates of dis-charge increase myocardial oxygen consumption; a careful balance must be reached.

10. Check entire system for loose connections

11. Anchor pacemaker wire to skin to prevent migration, clean point of entry, and apply dressing. To prevent inad-vertent manipulation of the pulse generator controls and its contamination by electroconductive fluids (internal or external), the pulse generator can be wrapped in a rubber surgical glove.

12. Obtain immediate chest films, posteroanterior and lat-eral. The catheter tip should be in the right ventricular apex. There should be no loop or tension angle left in the course of the catheter since straightening of the catheter will usually result in malpositioning and malfunction of the catheter.

B. Transthoracic cardiac pacing This mode of pacing is occa-sionally useful in emergency situations, usually during cardi-opulmonary resuscitation to treat cardiac standstill unrespon-sive to other measures. In this technique, insert a pacemaker wire with a flexible bent terminal end into the right ventricle through a long transthoracic needle that has been introduced into the right ventricle in the third or fourth left intercostal space. Then attach the pulse generator to the wire and begin pacing.

Although sometimes useful, this procedure disrupts ade-quate resuscitation and as such is often self-defeating. In the rare situations when the procedure is successful, subsequent

Complications 227

problems, including coronary artery laceration and pericardial tamponade, may prove to be insurmountable. The transthora-cic technique is not recommended in the majority of cases in which emergency pacing is needed, and it should probably be restricted to acute AV block during an arrest when P waves can be clearly seen on the ECG without QRS complexes that can be pharmacologically induced.

C. Temporary external cardiac pacing In this technique of pac-ing, place flat disk electrodes with an adequate amount of electrode paste on the patient's closed chest; these are held in place by a rubber chest strap. The anode is in the ECG V2 position; skin contact areas should be shaved and cleansed gently with an alcohol swab prior to application of the elec-trodes. Reapply generous amounts of electrode paste every 2 to 3 hours.

Thin-gauged 2.5-cm needle electrodes inserted in the skin have the advantages of lower voltage for pacing and fewer muscle contractions than seen with surface electrode pacing. Both battery-operated and AC-operated external cardiac pace-makers are available and supply electrical energies of 25 to 250 V to the closed chest wall over 2 to 3 msec, adequate to stimulate reasonably functioning myocardial tissue. Although this technique has proved useful in selected emergency situ-ations, it is rarely of benefit with severely damaged myocar-dium and will always be associated with chest discomfort and skin burns.

IV. COMPLICATIONS Complications of ventricular pacing are mul-tiple and estimated to occur in 15% to 20% of cases.

A. Complications related to the procedure of venous catheteri-zation Bleeding, thrombophlebitis, pneumothorax, hemo-thorax, wound infection, and embolization are examples. These have been listed in chapter 15 and will not be discussed here.

B. Complications related to temporary cardiac pacing

1. Ventricular arrhythmias induced during wire placement or caused by electrical leaks. Most occur when the catheter enters the right ventricle and will subside with moving the catheter or correction of leak. They are most serious in patients with acute myocardial infarctions. The defi-brillator should always be available at the bedside.

2. Perforation of right ventricle may occur with the straight or rigid catheter. It will result in hemopericardium and occasionally cardiac tamponade. The latter will require emergency therapy; otherwise the patient is managed con-

228 Temporary Ventricular Pacing

servatively by catheter repositioning and careful monitor-ing of the vital signs.

3. Breakage of catheter conductive element Pacemaker wire electrode integrity problems are best evaluated with the unipolar wire lead ECGs of both wire electrodes. A small, well-approximated wire fracture will sometimes show 60-cycle interference. A fully separated fracture will reveal a straight line. Short-circuiting between the wire electrodes will show identical proximal and distal unipolar ECGs, but the bipolar ECG will be isoelectric. Correction of an isolated wire fracture requires that the pacemaker be converted to a unipolar pacemaker by connecting the terminal of the intact wire electrode to the anode of the pulse generator and connecting the cathode of the pulse generator to the skin with either a disk skin electrode or a stainless steel suture. If adequate unipolar pacing can-not be obtained, the polarity of the system can be changed such that the wire electrode is connected to the cathode and the skin to the anode, since it is an observed fact that myocardial cells depolarize more easily when in contact with a positive charge.

4. Malposition of catheter This may be intraventricular or extraventricular. It is usually secondary to the inadequate initial placement of the catheter, its placement in the arm that with movement will advance the catheter, or to poor anchoring of the catheter at its point of entry into the skin.

Coronary sinus pacing can be recognized by the unipolar pacemaker wire ECG showing large P waves and a smaller QRS complex; during pacing, the paced beats on the surface ECG may show an RBBB pattern if the wire tip has migrated near the left ventricle through the coro-nary sinus. On chest roentgenograms, the wire tip will be seen to lie posteriorly. Correction requires repositioning of the catheter if adequate pacing is not occurring at this site.

Excessive right ventricular wedging is recognized by the unipolar wire lead ECG and shows a large current of in-jury without a deep S wave. Correction requires minor withdrawal of the wire until the optimal ECG is seen.

Perforation of the ventricle will result in loss of pacing and chest wall twitching or diaphragmatic stimulation. Confirm by roentgenogram and reposition the catheter, preferably under fluoroscopy.

5. Altered proper sensing and pacing threshold Abnormal demand function can present many problems. Undersen-sing can be caused by wire displacement, electrolyte dis-

References 229

turbance, pharmacologic agents, extension of myocardial infarction, or any disturbance that causes a low-amplitude bipolar sensing signal. Correction of these problems is di-rected at the cause and may require repositioning of the pacemaker wire, converting the bipolar system to a uni-polar system as described above, or using a different pulse generator with a higher input sensitivity.

Oversensing may be caused by interference or sensing P or T waves. This problem is usually corrected by decreas-ing the input sensitivity of the pulse generator.

6. Death during catheter insertion This may be due to the critical condition of the patient or the development of a fatal ventricular arrhythmia. In its most regrettable form it is an electrical death caused by the pacemaker whose function is not being closely monitored.

REFERENCES Cohen H.C., Arbel E.R.: Tachycardias and electrical pacing. Med. Clin. North Am. 60:343-367, 1976.

A review of the mechanisms of tachycardias and the indications for and the characteristics of electrical pacing that will lead to inter-ruption or suppression of the tachycardia or to ventricular slowing.

Lown B., Kosowsky B.D.: Artifical cardiac pacemakers. N. Engl. J. Med. 283:907-916, 971 -977 , 1023-1031, 1970.

A three-article series that provides considerable insight into the background and use of pacemakers.

Hindman M.C., Wagner G.S., JaRo M., et al.: The clinical signifi-cance of bundle-branch block complicating acute myocardial infarc-tion: II. Indications for temporary and permanent pacemaker inser-tion. Circulation 58:689-699, 1978.

A multicenter retrospective analysis of the experience with 432 pa-tients with myocardial infarction and bundle-branch block.

Wright K.E., Mcintosh H.D.: Artificial pacemakers: Indication and management. Circulation 57:1108-1118, 1973.

A brief review of the commonly employed pacemakers, the indica-tions for pacing, and some of the management problems encoun-tered.

Furman S., Escher D.J.W., Schwedel J.B., et al.: Transvenous pac-ing: A 7-year review. Am. Heart J. 71:408-416, 1966.

A brief review of the indications, technique, and complications based on experience with 110 patients.

Mabin-Uddin K., Smith P.E., Lombardo C., et al.: Percutaneous in-tracardiac pacing through the subclavian vein. J. Thorac. Cardio-vasc. Surg. 54:545-548, 1967.

One way of placing the catheter electrode. Schnitzler R.N., Caracta A.R., Damato A.N.: 'Floating' catheter for temporary transvenous ventricular pacing. Am. J. Cardiol. 31:351-354, 1973.

230 Temporary Vet, ' ig

The technique and results of placing a flow-directed balloon-tipped electrode catheter for right ventricular endocardial pacing.

Weinstein J., Gnoj J., Mazzara J.T., et al.: Temporary transve-nous pacing via the percutaneous femoral vein approach: A prospec-tive study of 100 cases. Am. Heart J. 8:695-705, 1973.

The title speaks for itself. The technique may be particularly useful in the patient with acute myocardial infarction.

Furman S.: Pacemaker emergencies. Med. Clin. North Am. 63:113-126, 1979.

A discussion of pacemaker emergencies and their proper therapy.

The following are a few of the comprehensive monographs on ven-tricular pacing that have appeared in the past decade. Samet P.: Cardiac Pacing: Clinical Cardiology Monographs. New

York, Grune & Stratton, 1973. Goldberger E.: Treatment of Cardiac Emergencies. St. Louis, C.V.

Mosby Co., 1974. Furman S., Escher D.J.W.: Modern Cardiac Pacing: A Clinical Over-

view. Bowie, Md., Charles Press Publishers, 1975. Luderitz B.: Cardiac Pacing. New York, Springer-Verlag New York,

1975. Varriale P., Naclerio E.A.: Cardiac Pacing: A Concise Guide to Clin-

ical Practice. Philadelphia, Lea & Febiger, 1979.

MEDICAL PROCEDURES MANUAL ' • ' t i •

by Garabed Eknoyan, M.D.

For the first time, the most important medical procedures are covered in a single, pocket-sized handbook, ready for clinical use.

Nineteen procedures are discussed in a clear, understandable manner, including concise and accurate information about how to perform each procedure . . . details of when and where not to proceed . . . ensuing complications . . . and interpretation. Add toi/this annotated references arid you have the idfeak companion to "hands-on" bedside experience and observation.

Each chapter is organized consistently: v \

• Indications • Contraindications • Technique

V • Complications • Interpretation

j Also, numerous line drawings help the novice envision the more / complicated procedures.

YEAR BOOK MEDICAL PUBLISHERS, INC. CHICAGO • LONDON