Case Studies NUR 7202 One and Two - Yolaashleysprofessionalportfolio.yolasite.com/resources/Case... · Web viewCASE STUDIES NUR 7202 ONE AND TWO21 Case Studies NUR 7202 One and Two

Running head: CASE STUDIES NUR 7202 ONE AND TWO 1

Case Studies NUR 7202 One and Two

Ashley Peczkowski

Wright State University

NUR 7202

CASE STUDIES NUR 7202 ONE AND TWO 2

Case Study One

1. What are potential etiologies of this patient’s symptoms?

Differential diagnoses for the patient’s symptoms are thyroid storm, migraine, meningitis,

and subarachnoid hemorrhage (SAH). The likelihood of diagnosis in order is as stated above

with thyroid storm being the most likely to be the causative agent to SAH being the least likely

cause. Each of the differential diagnoses need to be ruled in or out using information obtained

from history, physical exam, and tests results prior to beginning treatment to ensure safe and

effective therapy.

Thyroid storm also known as thyroid crisis or thyrotoxic storm is an increase in free

fraction thyroxine (T4) and triiodothyronine (T3). This occurs in one of four ways: the thyroid is

stimulated by trophic factors; there is activation of thyroid hormone synthesis and secretion

causing release of excess hormone; store of preformed hormone are excessively released due to

autoimmune, infectious, mechanical, or chemical cause; or exposure to extra-thyroid source of

thyroid hormone from either endogenous source such as struma ovarii or thyroid cancer, or

exogenous from factitious thyrotoxicosis (Bahn et al., 2011). Causes of this increase in thyroid

hormones can come from a variety of diseases such as Grave’s disease, toxic multinodular goiter,

subacute thyroiditis, or factitious thyrotoxicosis. If the patient has thyrotoxicosis

(hyperthyroidism) and is not diagnosed, then thyroid crisis may occur from common medical

events such as: anesthesia, stress, hypovolemia, pregnancy, labor, complicated deliveries,

excessive palpation of the thyroid, infection, burns, ketoacidosis, and food poisoning from

marine neurotoxin. The most common cause of thyroid crisis is from iodine increasing drugs.

These drugs include: radioactive iodine therapy, propylthiouracil therapy withdrawal, lithium

administration, stable iodine, iodinated contrast dyes, cytotoxic chemotherapy agents, aspirin


overdose, organophosphate intoxication, and amiodarone (Klubo-Gwiezdzinska & Wartofsky,

2012). The patients’ most likely cause was her pre-existing Graves disease that was exacerbated

by the administration of radioactive iodine (131I) therapy. Clinical signs include decompensated

organ systems resulting in high fevers out of proportion to any infection as a result of ineffective

auto thermoregulation from the hypothalamus or from increased basal metabolic rate with

increased oxidation of lipids; tachycardia out of proportion to fever or dysrhythmias such as

atrial fibrillation, supraventricular arrhythmias or ventricular arrhythmias without heart disease;

congestive heart failure or reversible dilated cardiomyopathy. Gastrointestinal disturbances such

as nausea, vomiting, and diarrhea from increased parasympathetic nervous system stimulation

are common, as well as central nervous system excitability which can lead to agitation,

confusion, emotional lability, paranoia, psychosis, status epileptics, stroke, coma, and basal

ganglia infarction (Klubo-Gwiezdzinska & Wartofsky, 2012).

Thyroid crisis is a complex disease that can be hard to diagnosis. Diagnosis is not based

on T3 levels since T3 levels can be normal and yet still have an increased T4 to T3 conversion.

This process is called euthyroid sick syndrome and is seen in thyroid hormone binding protein

disorders such as in pregnancy or with administration of drugs. Because of this, diagnosis is

based more on signs and symptoms and there severity. Several semiquantitative scales have been

designed to help practitioners’ diagnosis and treat thyroid crisis (Klubo-Gwiezdzinska &

Wartofsky, 2012). For other endogenous causes of hyperthyroidism, the best blood test to obtain

is a serum thyroid stimulating hormone (TSH) measurement. This measurement has the highest

sensitivity (98%) and specificity (92%) for hyperthyroidism or hypothyroidism. Normal TSH is

0.3-5.5 mU/L and is called euthyroid. Hyperthyroid TSH levels are less than 0.3 mU/L and

hypothyroidism TSH levels are greater than 5.6mU/L (Guidelines and Protocols Advisory


Committee, 2010). The TSH test is further enhanced by evaluating the free T4 level and plotting

the inverse log-linear relationship between the TSH and free T4. Apparent hyperthyroidism can

have serum blood levels of elevated free T4 and T3 with TSH levels that are non-detectable;

however, early hyperthyroidism may have normal serum T4 and free T4, elevated T3, and non-

detectable TSH. The latter is considered T3-toxicosis. Lastly, sub-acute hyperthyroidism may

show blood levels of normal serum free T4, normal T3 or free T3, and lower than normal TSH

levels (Bahn et al., 2011). The TSH, T4 and T3 are regulated by the hypothalamic-pituitary-

thyroid axis through a negative feedback loop (Guidelines and Protocols Advisory Committee,

2010).

One of the most obvious and notable physical signs of thyroid crisis are the cardiac

manifestations which presents as tachycardia, arrhythmias, and cardiomyopathies that develop

from high output states. This high output state results from a higher preload state from activation

of the renin-angiotensin-aldosterone axis, with a combination of reduced afterload from the

increased T4 relaxing effects on endovascular muscle cells. This dyssynchrony results in systolic

hypertension with a widened pulse pressure. In combination with vomiting and diarrhea, volume

depletion with hypotension and vascular collapse leading to shock can also occur. Further

disruption from the high output state results in increased myocardial oxygen demands,

myocardial infarction, and pulmonary hypertension. This excitability state that is induced also

affects the hematological components of the body by causing leukocytosis with a shift to the left

without the presence of infection. The inflammatory cascade is initiated and results in a

hypercoagulability state. Associated factors from this include increased fibrinogen, factors VIII,

factors IX, tissue plasminogen activator inhibitor one, von Willebrand factors, and an increased

red blood cell mass. This hypercoagulability state leads to thrombosis formation which in turn


can lead to pulmonary embolism and can either be the cause of or exacerbate the pulmonary

hypertension. Other respiratory complications include respiratory failure from tachypnea from

increased oxygen demands (Klubo-Gwiezdzinska & Wartofsky, 2012).

Besides nausea, vomiting and diarrhea, the patient may experience abdominal pain from

delayed gastric emptying. The delay is caused by disruption in the neurohormonal regulation

affecting the gastric myoelectrical activity. Hepatic damage can also occur from increased

anaerobic metabolism and glycogenolysis which is used to create lactic acid. The increased lactic

acid damages the hepatic cells leading to increased lactate dehydrogenase, aspartate

aminotransferase, bilirubin, and alkaline phosphatase. The increased in alkaline phosphatase

however is the result of increased osteoblastic activity in the bone and not hepatic damage. This

results in increased serum calcium levels as well as a metabolic increase of ketones producing

acidosis. Hyperglycemia is present in the beginning from the glycogenolysis and catecholamine-

mediated insulin release blockade with increased renal clearance and body resistance. Once

glycogen stores are depleted hypoglycemia occurs. Lastly renal dysfunctions occur from

glomerulosclerosis and proteinuria from increased glomerular filtration rate; renal failure from

rhabdomyolysis; urinary retention from detrusor and bladder dysfunction; and autoimmune

complex-mediated nephritis (Klubo-Gwiezdzinska & Wartofsky, 2012). This patient is most

likely to have thyroid crisis based on the history and physical findings of recent Grave

hyperthyroidism diagnosis, chronic right upper quadrant pain, and a recent weight loss of 30

pounds.

Migraine is the second most likely diagnosis for this patient’s headache. Migraines are

usually a hereditary disorder related to genetic predisposition (Silberstein & Dodick, 2013).

There are two different theories on migraine development: one being cortical spreading


depression (CSD) and the other brainstem generator. The theory of CSD is the main theory of

thought behind migraines with auras. This is based on studies conducted on rats and pigeons

where brain mapping was completed and then stimuli introduced with monitored response of the

brains neural activity. The observation demonstrated that the aura before the migraine is the

result of cortical neuronal activation immediately followed by postictal depression of the

neuronal firing. The process is responsible for meningeal pain brought on by neurogenic

inflammation, vasodilation, and manipulation of the blood brain barrier resulting in plasma

protein extravasation. Manipulation of the blood brain barrier is obtained through activation of

the brain matrix metalloproteinases which are responsible to opening the blood brain barrier to

large molecule such as proteins (Estemalik & Tepper, 2013). The CSD wave of depression of

neurons followed by a longer wave of inhibition runs at a rate of three to six mm/minute in

multiple areas of the brain including the cerebellum, cortex, and hippocampus. This rate of speed

is important because it is much slower than normal brain activity and causes large changes in

ionic concentrations. This self-propagating wave of depolarization of the neuronal and glial cells

is activated by potassium influx, glutamate influx, and sodium/potassium pump activation. This

process helps neurologist understand which drugs can help prevent and stop an acute migraine

attack. The unnecessary activation of these pumps is responsible for activation of central and

peripheral trigemionvascular nociceptive pathways and thus pain outside of the meningeal

irritation through vasodilation and neurogenic inflammation caused by release of inflammatory

cytokines, neuroinflammatory peptides, and calcitonin gene-related peptide (Costa et al., 2013).

Non-aura migraines are more difficult to understand and therefore treat. This is based on

the brainstem generator theory where there is a dysfunction in the brainstem nuclei that are

responsible for central control of nociception. This dysfunction causes increased regional


cerebral blood flow and activation of the trigeminal nerve. Others argue that this increase is the

result of pain perception or increased activity of endogenous antinociceptive system. No matter

what the cause of the increased cerebral blood flow, the dysfunction on the brainstem generator

could either trigger a migraine or add to the central excitability of the trigeminal pathways

(Pietrobon & Striessnig, 2003). Although this patient meets criteria for migraine and has a

history of migraines, given the recent diagnosis of Grave hyperthyroidism and fever thyroid

crisis is more likely.

The third most likely cause of the patient’s migraine is meningitis. Meningitis is mostly

caused by either a bacterial infection (Streptococcus pneumoniae, Haemophilus, influenza type

b, and Neisseria) or viral infection (Entrovirus). Despite the causative agent the immune system

responds to the infection by attacking the organism in the subarachnoid space thus releasing

cytokines and initiating the inflammatory cascade. The introduction of cytokines results in

increased permeability of the blood brain barrier to allow leukocytes to enter for phagocytosis.

This however, also allows large protein molecules to enter the meninges; creating interstitial

edema. This in combination with cerebral vasculitis and systemic hypotension results in cellular

hypoxia and death. The most common finding with meningitis is a severe headache, nuchal

rigidity, sudden high fever, photophobia, phonophobia, confusion, and irritability. Common

assessment tests include Brudzinski’s sign, Kernig’s sign, and nuchal rigidity. Brudzinski’s and

Kernig’s sign both have a sensitivity of 5% with a likelihood ratio 0.97. Nuchal rigidity is more

accurate with a sensitivity of 30% and a likelihood ration of 0/94. (Grandgirard et al., 2013;

Mohseni & Wilde, 2012). This diagnosis is less likely based on the absent neck stiffness and

transient fever.


Finally the diagnosis of subarachnoid hemorrhage (SAH) should be considered. This is

the least likely cause because the symptoms of the patient do not directly fit the symptoms of

SAH; however, because of its high mortality rate, SAH should be considered. A SAH results

from a rupture in a thinned artery in the subarachnoid space. This thinning can be caused by

smoking, hypertension, drug or alcohol abuse, lower BMI, first degree relative with SAH, or

connective tissue disorders. At risk patients include older adults, women, or African Americans

or Hispanics. This sudden rupture of an aneurysm causes a severe sudden headache commonly

referred to as a thunder clap headache and meningeal irritation symptoms such as photophobia,

blurred vision, nausea, vomiting, nuchal rigidity, confusion, or altered level of consciousness. A

SAH is considered a medical emergency and needs immediate treatment (Rank, 2013). This

diagnosis is the least likely based on the gradual onset, “hammering” pain, and absent

neurological symptoms.

2. Which of the following is not considered a diagnostic criterion of thyroid storm?

A. Nausea and vomiting

B. Tachycardia

C. Tremor

D. Fever

E. Pulmonary edema

Of the listed symptoms tremors are the only one that is not on the diagnostic criteria list

for thyroid storm. The diagnostic criteria for thyroid storm include degrees of elevated

temperature; central nervous system effects such as agitation, psychosis, seizures, and coma;

gastrointestinal upset such as nausea, vomiting, diarrhea, and jaundice; tachycardia, congestive

heart failure symptoms, and atrial fibrillation with or without precipitating factors. These


symptoms were discussed in detail previously. A point number is assigned to each of the

following symptoms and there severity. After a thorough assessment is completed, the

practitioner will add up the following points awarded to each category and severity. A score of

45 or greater is highly indicative of thyroid storm while a score between 25 and 44 suggests

impending storm and a score less than 25 indicates that a thyroid storm is unlikely (see table 1).

The chart was designed to help practitioners delineate between thyrotoxicosis, an abnormal

amount of thyroid hormone concentration, and thyroid storm; which is the extreme state of

thyrotoxicosis. There is no direct point at which thyrotoxicosis becomes a thyroid storm and

treatment should begin early in thyrotoxicosis before the advancement of thyroid storm (Nayak

& Burman, 2006).

The thyroid is responsible for setting the body’s metabolic rate and in thyroid storm this

metabolic rate is drastically increased. The thyroid hormone also increases the density of beta-

adrenergic receptors which enhance the effects of the catecholamines creating a stress response

by the body. In the brain the thyroid hormone affects the myelination of the oligondendroglial

cells and the myelin membrane. Excess thyroid hormones can cause demyelination and myelin

membrane disruptions, inhibiting transmission. Along with affecting myelination these hormones

are also responsible for increasing synaptic transmission, increasing the pain receptors, and

increasing neurotransmitters such as serotonin and norepinephrine. The increase in synaptic

transmission, pain receptors, and neurotransmitters, will in turn increase neuroelectrical activity.

Because of these two seemly opposite effects, a person with thyroid storm can experience one

extreme, such as coma, to the other, such as with seizures or psychosis. While fine hand tremors

are a common finding in hyperthyroidism they are not a constant finding in thyroid storm and are

therefore not considered part of the diagnostic criteria. More common signs included on the


diagnostic criteria are the nausea, vomiting, tachycardia, fever, and pulmonary edema for reasons

previously stated.

3. Based on the patient’s symptoms and diagnostic studies, which of the following

management strategies is not appropriate?

A. Abaltion with 1311 (RAI)

B. Thyroidectomy

C. Beta-blocker and a thionamide

D. Lugol solution

E. Corticosteroids

Thyroidectomy, beta blockers, thionamide drugs, and Lugol solution are indicated in the

treatment of thyroid storm. Ablation with the use of 131I is not indicated for the treatment of

thyroid storm because this increases the amount of thyroid hormone synthesis, further increasing

the severity of the thyroid storm. Ablation with 131I has been used for decades for the treatment

of hyperthyroidism and is mostly well tolerated. The medication is only indicated for patients

who have been given thionamide drugs before treatment and have obtained a euthyroid state.

This is because in some cases administration of 131I alone while increase the amount of free T4

thus further worsening the thyroid storm. Those at greatest risk include patient who are

extremely symptomatic, elderly, in atrial fibrillation, heart failure, have pulmonary hypertension,

in renal failure, have an infection, suffered a trauma, have poorly controlled diabetes, or have

cerebrovascular or pulmonary diseases. Treatment with ablation 131I is indicated if the patient

has been pre-treated with a thionamide before and after administration and are otherwise healthy

(Bahn et al., 2011).


Treatment for thyroid storm is aimed at stopping thyroid hormone synthesis, release of

stored hormone, prevention of T4 to T3 conversion, and controlling peripheral effects such as

adrenergic symptoms and systemic decompensation. This is completed through administration of

several drugs for a multimodal effect. Not only is it important to use multiple medications but

also the order and timing of medications is crucial. It is important to start treatment with

thionamide first before treating with iodine therapy to prevent increased thyroid hormone

synthesis. Starting with a thionamide drug such as propylthiouracil or methimazole first causes

inhibition of the thyroperoxidase-catalyzed coupling process. This prevents iodotyrosine residues

from combining to create T3 and T4. Other important benefits of thionamides are that they

prevent thyroid follicular cell function and growth; cause an immunosuppressive effect by

decreasing antithyrotropin-receptors, intracellular adhesion molecule one, and soluble interleukin

two; cause apoptosis of intrathyroidal lymphocytes and reduce HLA antigen expression. While

methimazole is prescribed most because of its longer half-life and therefore reduced dosing

frequency; propylthiouracil has the added benefit of inhibiting T4 to T3 conversion in the

peripheries. These drugs are given as propylthiouracil 200-300mg oral every six hours or

methimazole 20-25mg oral every six hours until stable and then can be given 80-100mg orally

once to twice a day. Both of these drugs can also be given rectally if the patient is comatose or

methimazole can be given intravenously. Important side effects are abnormal taste, pruritus,

urticaria, fever, arthralgia, agranulocytosis, hepatotoxicity, and vasculitis (Nayak & Burman,

2006). According to the Ohio Board of Nursing an acute care nurse practitioner may prescribe

these drugs without limitation (Ohio Board of Nursing, 2013).

Once the anti-thyroid medications have inhibited new thyroid hormone synthesis the

medical treatment is then focused on reducing thyroid secretion of stored hormone. Iodine or


lithium is used to prevent proteolysis of colloids and secretion of T4 and T3 into the peripherals.

Timing of administration is again very important. Iodine solution, called Lugol solution, should

not be given within the first hour of thionamide administration because if the thyroid has not

been adequately blocked then the iodine will increase thyroid hormone synthesis, hormone

stores, and further increase thyrotoxicosis. When given correctly Lugol solution greatly

decreases serum T4, reducing levels to normal in four to five days. If the patient is allergic to

iodine then lithium can be substituted at 300mg orally every six hours. Lugol solution is given

either orally or as a saturated solution of potassium iodine given at three to five drops every six

hours (Klubo-Gwiezdzinska & Wartofsky, 2012). According to the Ohio Board of Nursing an

acute care nurse practitioner may prescribe these drugs for thyrotoxicosis (Ohio Board of

Nursing, 2013).

Thyroid hormone suppression is not enough for treatment of thyroid storm because there

remain large amounts of circulating hormone in the peripherals. Other treatments including

plasmapheresis or therapeutic plasma exchange with albumin to increase bound thyroid

hormone, are quick fixes for acute emergency but only have therapeutic effects for 24-28 hours

(Klubo-Gwiezdzinska & Wartofsky, 2012). Controlling systemic effects of thyrotoxicosis is the

main supportive treatment while waiting for systemic hormone levels to equalize. Cardiovascular

effects of thyroid storm are controlled by the administration of beta-blockers. Propranolol 60mg

to 120mg orally every four hours or parenterally at 0.5mg to one mg bolus over ten minutes and

then one to three mg over ten minutes every few hours as needed is most commonly prescribed.

Esmolol 50-100µg/kg/min is also indicated for treatment as an alternative for acute thyroid

storm. Other beta-blockers used are atenolol, metoprolol, and nadolol. Because of the increase in

metabolism and increased amount of cardiac beta-adrenergic receptors, larger doses are needed


for beneficial effect. Propranolol as the added benefit of reducing T3 levels by up to 30%.

Because atrial fibrillation is common in thyrotoxicosis anticoagulation is recommended based on

stroke risk factors. Lower doses of warfarin are needed because of the increased metabolism of

vitamin K-dependent clotting factors. Finally, glucocorticoids are indicated for treatment because

they reduce the peripheral conversion of T4 to T3 and also used to treat adrenal insufficiency,

which is commonly seen in thyroid storm (Nayak & Burman, 2006). According to the Ohio

Board of Nursing beta blockers, warfarin, and glucocorticoids can all be prescribed by an acute

care nurse practitioner (Ohio Board of Nursing, 2013). Lastly surgical treatments such as early

thyroidectomy have been used with success greatly reducing the mortality rate (Klubo-

Gwiezdzinska & Wartofsky, 2012).


Case Study Two

1. What is the most appropriate next step in this patient’s diagnostic evaluation?

A. Contrast-enhanced CT scan of the brain

B. Magnetic resonance imaging (MRI) of the brain

C. Lumbar puncture (LP) with cerebrospinal fluid (CSF) analysis

D. Electroencephalogram

E. No further diagnostic testing

Meningitis should be suspected in all patients with altered mental status, fever, and neck

stiffness. Because of the patient’s age and symptoms, it is appropriate to obtain a stat head non-

contrast head cat scan (CT) for evaluation of an acute hemorrhagic stroke. It is also an important

evaluation test to determine the patient’s risk of herniation during a lumbar puncture. Even if the

CT is normal there is still a risk for herniation. Signs associated with increased risk of herniation

include deteriorating level of consciousness, signs of brainstem involvement, and a recent seizure

(Tunkel et al., 2004). Once this immediate evaluation has been completed, the next step is to

perform a lumbar puncture to test for meningitis. A cerebral spinal fluid (CSF) culture is

considered to be the gold standard for bacterial meningitis diagnosis. Other tests are needed to

help confirm the diagnosis and also support antibiotic treatment. These tests include serum

inflammatory marker, blood cultures, skin biopsy, and urine antigen. The purpose of the lumbar

puncture is to test to CSF for signs of bacterial meningitis such as polymorphonuclear

pleocytosis, hypoglycorrhachia, and raised CSF protein levels. This also helps tests for viral

meningitis versus bacterial. Bacterial meningitis has glucose levels in the CSF of less than

1.9mmol per liter, CSF glucose to blood glucose ratio of 0.23, protein concentration greater than

2.2g per liter, and a leukocyte level more than 2,000 per mm3. However, if protein levels are less


than 0.5g per liter and leukocytes less than 100 per mm3, bacterial meningitis can still be

present. CSF cultures are used to grow the bacterial to levels that are then identifiable for

treatment. Once the correct organism has been identified then the best treatment can be initiated.

It is important to perform the lumbar puncture before empiric treatment with antibiotics is

initiated because detection level before treatment in a large case series was 88-70% while post

antibiotic treatment was at 66-62% (Brouwer, Tunkel, & Beek, 2010).

The most common pathogens for bacterial meningitis in the adult population is the

community acquired Steptococcus pneumoniae and Neisseria meningitidis. For these two main

bacterial pathogens the sensitivity of a lumbar puncture for a CSF gram stain is 69-93% for S.

pneumoniae and 30-89% for N. meingitidis. Because of this it is recommended that blood

cultures, latex agglutination test, and PCR are also obtained. Blood cultures are used to detect the

organisms if the CSF cultures are negative. The blood culture tests are 60-90% sensitivity for S.

pneumoniae and 40-60% for N. meningitidis. Latex agglutination test is used when bacterial

meningitis is suspected but CSF cultures are negative. This is performed by testing serum

containing bacterial antibodies against capsular polysaccharides in the meningitis bacteria. This

test is known to only take 15 minutes and has a sensitivity level of 78-100%. Lastly a PRC is

performed to detect the presence of meningitis bacteria DNA in the CSF. The sensitivity of this

test is 61-100% in S. pneumoniae and 88-94% for N. meningitidis (Brouwer et al., 2010).

A Magnetic resonance imaging (MRI) of the brain is not indicated in this patient because

of the altered mental status. Early treatment is needed in patients with altered mental status to

reduce mortality rates. The longer the delay, the higher the mortality rate and waiting on an MRI

can take hours to even days. A MRI is useful in early meningitis before the bacteria have

replicated enough to show positive results in the blood and CFS. A MRI can see abnormal


meningeal enhancement early in the process however once the patient has experienced altered

mental status the inflammatory damage is great enough to be seen in regular testing (Kamra et

al., 2004).

A contrast-induced CT scan of the brain is used to monitor complications of meningitis

and not for initial diagnosis. A contrast-induced CT scan can evaluate for hydrocephalus,

subdural effusion, empyema, infarction, parenchymal abscess, or ventriculitis. This type of CT

can be normal in a patient with bacterial meningitis and therefore should not be used for

diagnosis. Lastly, an electroencephalogram can be used to detect abnormal brain waves seen in

meningitis but cannot be used to diagnose (Hughes, Raghavan, Mordekar, Griffiths, & Connolly,

2010).

2. Which of the following is this patient’s most likely diagnosis?

A. Viral meningitis

B. Fungal meningitis

C. Bacterial meningitis

D. Mycobacterial meningitis

E. Noninfectious meningeal irritation

The most likely diagnosis of this patient is bacterial meningitis. There are five different

types of meningitis including: bacterial, viral, parasitic, fungal, and non-infectious. Bacterial

have become more uncommon with the use of vaccinations and include the two main types: S.

pneumoniae and N. meningitidis. Viral infections have a lower mortality rate, are more common,

and include mainly enterococcus but also syphilis. Fungal infections are rare unless the patient is

immunocompromised with either: HIV, diabetes, transplant recipient, or other

immunocompromising conditions. Parasitic infects are common in third world countries and


should be considered only in the patient has recently travel to a third world country. Lastly, non-

infectious meningitis is cause by a comorbidity, rather than an organism, such as lupus or types

of brain surgery (CDC, 2013).

The normal opening pressure of an adult should range from 60 to 250 mm H2O and

therefore anything over 250 is considered to be intracranial hypertension. Intracranial

hypertension is indicative of a pathological state including meningitis, intracranial hemorrhage,

and tumors. If a lumbar puncture is performed, the practitioner should remove the CFS slowly

and the pressure should be monitored. The lumbar puncture should be stopped once the pressure

level is about 50% less than the original pressure. An elevated opening pressure is commonly

seen in bacterial meningitis and not in viral meningitis. Next the color of the CSF should be

analyzed. Clear CSF is normal but turbid CSF is the result of abnormal findings such as

hemoglobin and leukocytes. Another term is called xanthochromia, in which the CFS is yellow,

orange, or pink from breakdown of hemoglobin into oxyhemaglobin, methamoglobin, and

bilirubin. This can be caused by a variety of conditions such as meningitis or subarachnoid

hemorrhage. Lastly the contents of the CSF are examined to revile the number of leukocytes, red

blood cells, protein level, and glucose level. This patient most likely has bacterial meningitis

because her CSF count has the indications of bacterial meningitis. Bacterial meningitis typically

has an elevated opening pressure, a leukocyte count higher than 1,000 per mm3, mild or marked

elevation in protein levels, and a normal to decreased CFS glucose level to serum glucose level

ration. This patient has all of the above and despite her CSF glucose being normal it is greatly

decreased compared to her serum glucose level (Seehusen, Reeves, & Fomin, 2003).

3. Based on the Gram stain, which of the following antibiotic regimens is most

appropriate in this patient?


A. Penicillin G

B. Ceftriaxone

C. Ceftriaxone and Vancomycin

D. Ampicillin and cefotaxime

E. Cefepime

This patient is above the age of 50 and has a history of diabetes she most likely suffers

from Streptococcus pneumoniae meningitis. S. pneumoniae is most commonly seen in patients

under the age of two, older than 50 years of age, or have co-morbidities such as: splenectomy,

multiple myeloma, hypogammaglobulinemia, alcoholism, chronic liver or kidney disease,

cancer, Wiskott-Aldrich syndrome, thalassemia, diabetes, basilar skull fracture, or cochlear

implant with positioners. This diagnosis is further supported by the gram stain that showed

Gram-positive cocci pairs, many polymorphonuclear leukocytes, and few mononuclear cells. In

up to 60% of pneumococcal meningitis there is a distant source of infection such as pneumonia,

otitis media, sinusitis or endocarditis in which a consulted otorhinolaryngologist is

recommended. Pneumococcal meningitis is a life threatening disease that can cause a meningitis

triad of high fevers, nuchal rigidity, and altered mental status in up to 60% of cases. This can

also present with a high rate of abnormal brain dysfunction presenting in focal neurological

abnormalities (40%), seizures (25%), and coma (one in five admissions) (Brouwer et al., 2010).

Pneumococcal meningitis used to be treatable with penicillin but the overuse of antibiotics has

caused many cases to become penicillin resistant pneumococcal meningitis. Because of this it is

recommended to started empiric treatment, based on the gram stain, with Vancomycin and an

expanded-spectrum cephalosporin like ceftriaxone. This is based on current antimicrobial


susceptibility patterns and the assumption that the organism is antimicrobial resistant. This drug

regimen should be continued until CSF cultures identify the organism, at which time the drug

regimen should be changed based on the presenting organism. Treatment is recommended for ten

to 14 days once pathogen has been isolated (Tunkel et al., 2004). According to the Ohio Board of

Nursing an acute care nurse practitioner may prescribe both antibiotics (Ohio Board of Nursing,

2013).

4. Complete the following table.

Table 1

Cerebrospinal Fluid Analysis in MeningitisMeasurement Normal Bacterial

Meningitis

Viral

Meningitis

Fungal

Meningitis

Parasitic

Meningitis

Opening

Pressure

(mmH20)

70-180 Markedly

Elevated

Usually

Normal to

Slightly

Elevated

Variable;

Moderately

Elevated

Normal to

Slightly

Elevated

WBCs 0-5

Lymphocytes

≥1,000 per

mm3

Polymorphic

Neutrophils

<100 per

mm3

Lymphocytes

Variable;

100-1,000

per mm3

Lymphocytes

Variable;

100-1,000

per mm3

Lymphocytes

Glucose (mg/dL) 45-85 Normal to

Decreased

Usually

Normal to

Decreased

Decreased Normal

Protein (mg/dL) 15-45 Mild to Normal to Elevated Elevated


Marked

Elevation

Elevated

Modified from: (1). Seehusen, D., Reeves, M., & Fomin, D. (2003). Cerebrospinal fluid analysis.

American Family Physician, 68(6), 1103-1109. Retrieved from

http://www.aafp.org/afp/2003/0915/p1103.html (2). McAuley. (2013). Cerebrospinal Fluid

(CFS) analysis- meningitis. GlobalRPh: The Clinician’s Ultimate Reference. Retrieved from

http://www.globalrph.com/cerebrospinal_fluid.htm. (3). Hancock. (2005). Lab values and

analysis. The Practitioner’s Pocket Pal. Miami: MedMaster.

5. Should this patient receive adjuvant therapy with dexamethasone?

Dexamethasone is indicated for adjunctive treatment for pneumococcal meningitis to

reduce inflammation as recommended by Infectious Disease Society of America, European

Federation of Neurological Sciences and British Infection Society (Brouwer et al., 2010).

Dexamethasone reduces pro-inflammatory cytokines, monocytes, dendritic cells, astroglial cells,

neutrophils, reactive oxygen substances, leukocyte adherence, and increases anti-inflammatory

cytokines. Neurological damage that occurs during meningitis is not the result from the pathogen

but for from the inflammatory cascade induced by the pathogen. Dexamethasone decreases the

amount of nitric oxide (NO) and tumor necrotizing factor alpha (TNF-α) produced from

astroglial cells that have been stimulated by pneumococcal cell wall. This combined with

endothelial cell reduction in TNF-α, inter-lukin-1 (IL-1), and mononuclear cell inhibition of S.

pneumoniae-induced IkBk phosphorylation and degradation of the binding of NF-kB to DNA.

This results in the reduction of the inflammatory cascade. Reduction in inflammation in the brain

results in lower intracranial pressure, brain edema, altered cerebral blood flow, cerebral

vasculitis, neuronal injury, and CSF pleocytosis (Mook-Kanamori, Geldhoff, Poll, & Beek,


2011). Dexamethasone in addition to antibiotics has shown to reduce hearing loss and other

neurological sequelae however did not show any significant benefit in overall mortality rate. This

drug is recommended by infectious disease to be ordered on all patients with suspected or proven

pneumococcal meningitis and continued if the CSF stain shows gram-positive diplococci or if

blood or CSF cultures produce S. pneumoniae. Dexamethasone is given at the recommended

dose of 0.15mg/kg every six hours for two to four days intravenously with the first dose given

right before or with the first dose of antibiotics (Tunkel et al., 2004). According to the Ohio

Board of Nursing, acute care nurse practitioners have prescriptive authority to order

dexamethasone (Ohio Board of Nursing, 2013). Controversies on giving dexamethasone include

prohibiting Vancomycin therapy to penetrate into the CSF by reducing meningeal inflammation

and also possibly causing hippocampus apoptosis without cognitive impairment which can also

be caused by S. pneumoniae infections. Despite these concerns the benefits out way the risk and

dexamethasone is recommended for all patients with confirmed for suspected pneumococcal

meningitis even if the pathogen is suspected of being highly resistant to penicillin and

cephalosporins (Mook-Kanamori, Geldhoff, Poll, & Beek, 2011; Tunkel et al., 2004).


References

Bahn, J., Burch, H., Cooper, D., Garber, J., Greenlee, M., Klein, I., ... Stan, M. (2011).

Hyperthyroidism and other causes of thyrotoxicosis: Management guidelines of the

American Thyroid Association and American Association of Clinical Endocrinologist.

Thyroid, 21(6), 593-647. http://dx.doi.org/10.1089/thy.2010.0417

Guidelines and Protocols Advisory Committee. (2010). Thyroid function tests in the diagnosis

and monitoring of adults. The Clinical Practice Guidelines. Retrieved from

http://www.bcguidelines.ca/guideline_thyroid.html

Brouwer, M., Tunkel, A., & Beek, D. (2010). Epidemiology, diagnosis, and antimicrobial

treatment of acute bacterial meningitis. Clinical Microbiology Reviews, 23(3), 467-492.

http://dx.doi.org/10.1128/CMR.00070-09

Center for Disease Control and Prevention. (2013). Meningitis. National Center for

Immunization and Respiratory Diseases. Retrieved from

http://www.cdc.gov/meningitis/index.html

Costa, C., Tozzi, A., Rainero, I., Maria, L., Calabresi, P., Ayata, C., & Sarchielli, P. (2013).

Cortical spreading depression as a target for anti-migraine agents. The Journal of

Headache and Pain, 14(62), 1-39. http://dx.doi.org/10.1186/1129-2377-14-62

Estemalik, E., & Tepper, S. (2013). Preventive treatment in migraine and the new US guidelines.

Neuropsychiatric Disease and Treatment, 709-720.

http://dx.doi.org/10.2147/NDT.S33769

Grandgirard, D., Gaumann, R., Coulibaly, B., Dangy, J., Sie, A., Junghanss, T., ... Leib, S.

(2013). The causative pathogen determines the inflammatory profile in cerebrospinal


fluid and outcome in patients with bacterial meningitis. Mediators of Inflammation, 1-12.

http://dx.doi.org/10.1155/2013/312476

Hancock, J. (2005). Lab values and analysis. In The Practitioner’s Pocket Pal (2nd ed.) pp. 5-6.

Miami: MedMaster Inc

Hughes, D., Raghavan, A., Mordekar, S., Griffiths, P., & Connolly, D. (2010). Role of imaging

in the diagnosis of acute bacterial meningitis and its complications. Postgraduate

Medical Journal, 86(1018), 478-485. http://dx.doi.org/10.1136/pgmj.2010.097022

Kamra, P., Azad, R., Prasad, K., Jha, S., Pradham, S., & Gupta, R. (2004). Infectious meningitis:

Prospective evaluation with magnetization transfer MRI. British Journal of Radiology,

77, 387-394. http://dx.doi.org/10.125/bjr/23641059

Klubo-Gwiezdzinska, J., & Wartofsky, L. (2012). Thyroid Emergencies. Medical Clinics of

North America, 96, 385-403. http://dx.doi.org/10.1016/j.mcna.2012.01.015

McAuley, D. (2013). Cerebrospinal fluid (CSF) analysis- meningitis. GlobalRPh: The

Clinician’s Ultimate Reference. Retrieved from

http://www.globalrph.com/cerebrospinal_fluid.htm

Mohseni, M., & Wilde, J. (2012). Viral meningitis: Which patients can be discharged from the

emergency department?. The Journal of Emergency Medicine, 43(6), 1181-1187.

http://dx.doi.org/10.1016/j.jemermed.2012.03.021

Nayak, B., & Burman, K. (2006). Thyrotoxicosis and thyroid storm. Endocrinology and

Metabolism Clinics of North America, 35, 663-686.

http://dx.doi.org/10.1016/j.ecl.2006.09.008

Ohio Board of Nursing. (2013). The formulary developed by the committee on prescriptive

governance. Ohio Board of Nursing, 1-36. Retrieved from www.nursing.ohio.gov


Pietrobon, D., & Striessnig, J. (2003). Neurobiology of migraine. Nature Reviews: Neuroscience,

4, 386-399. http://dx.doi.org/10.1038/nrn1102

Rank, W. (2013). Aneurysmal subarachnoid hemorrhage. Nursing 2013, 42-51. Retrieved from

www.Nursing2013.com

Seehusen, D., Reeves, M., & Fomin, D. (2003). Cerebrospinal fluid analysis. American Family

Physician, 68(6), 1103-1109. Retrieved from

http://www.aafp.org/afp/2003/0915/p1103.html

Silberstein, S., & Dodick, D. (2013). Migraine genetics- A review Part I. Headache: The Journal

of Head and Face Pain, 1-11. http://dx.doi.org/10.1111/head.12156

Tunkel, A., Hartman, B., Kaplan, S., Kaufman, B., Roos, K., Scheld, M., & Whitley, R. (2004).

Practicing guidelines for the management of bacterial meningitis. Clinical Infectious

Diseases, 39, 1267-1284. Retrieved from http://cid.oxfordjournals.org


Table 1

Thyroid Storm Diagnostic Criteria

Diagnostic Parameters Scoring Points

Thermoregulatory Dysfunction

Temperature

99-99.9 5

100-100.9 10

101-101.9 15

102-102.9 20

103-103.9 25

≥104.0 30

Central Nervous System Effects

Absent 0

Mild (Agitation) 10

Moderate (Delirium, Psychosis, Extreme

Lethargy)

20

Severe (Seizures, Coma) 30

Gastrointestinal-Hepatic Dysfunction

Absent 0

Moderate (Diarrhea, Nausea, Vomiting,

Abdominal Pain)

10

Severe (Unexplained Jaundice) 20

Cardiovascular Dysfunction


Tachycardia

90-109 5

110-119 10

120-129 15

≥140 25

Congestive Heart Failure

Absent 0

Mild (Pedal Edema) 5

Moderate (Bibasilar Rales) 10

Severe (Pulmonary Edema) 15

Atrial Fibrillation

Absent 0

Present 10

Atrial Fibrillation with Precipitating Event

Absent 0

Present 10

Table 1. Adapted from: (1) B. Nayak & K. Burman. (2006). Thyrotoxicosis and thyroid storm.

Endocrinology and Metabolism Clinics of North America, 32, 663-686.

Documents

Case Studies NUR 7202 One and Two - Yolaashleysprofessionalportfolio.yolasite.com/resources/Case... · Web viewCASE STUDIES NUR 7202 ONE AND TWO21 Case Studies NUR 7202 One and Two