SGD: SPINEA Cautionary

TaleBLOCK 5

GENERAL DATA

ALANGILAN, Ronalyn21/FNursing StudentRight-handedSta. Ana Manila

DOA: October 1, 2009

HISTORY of PRESENT ILLNESS

2 months PTA(+) nape pain, VAS 4-5/10(+) fatigue; (+) easy fatigability(-) sensory deficits(-) bowel and bladder incontinence

(+) Consult with private MD unrecalled meds, no relief

HISTORY of PRESENT ILLNESS

2 weeks PTA(+) bilateral LE weakness, left first then right(+) difficulty in ambulation - community ambulator(-) sensory deficits(-) bowel and bladder incontinence

(+) Consult with albularyo no relief

HISTORY of PRESENT ILLNESS

1 week PTA(+) bilateral LE numbness(+) constipation(+) urinary retention(+) difficulty in ambulation - home ambulator with help

HISTORY of PRESENT ILLNESS

1 day PTA(+) consult at PGH ED

foley catheter inserted; for OPD ff-up

HISTORY of PRESENT ILLNESS

On day of admission(+) consult at PGH ED; laboratories and imaging done admitted at spine unit-Pay.

ROS: (-) weight loss, (-) cough and colds, (+) intermittent fever lysed with paracetamol, (+) slight DOB; (+) malaise, (+) easy fatigability, (+) dysuria, (+) urinary retention, (-) night sweats (+) constipation, (-) Hx of trauma

PAST MEDICAL HISTORY

(+) PTB exposure – schoolNo previous hospitalizationsNo food or drug allergies

FAMILY MEDICAL HISTORY

(-) PTB (+) HTN – father (-) DM, BA, CA, goiter, liver disease, kidney

disease, heart disease

PERSONAL SOCIAL PROFILE

No vices2nd year nursing student with ward and local

health center exposure1 non-promiscuous sexual partnerLives at home with mother and sibling in a 2-

storey building; father works abroad as a seaman

PE on ADMISSION

Stretcher-borne, awake, coherent, NICRDBP 110/70 HR 76 RR 20 Temp afebrileAS, PC, (-) CLAD, (-) NVE, (-) ANMECE, CBS, (-) r/wAP, DHS, NRRR, (-) murmurSoft, flabby, nontender abdomen, NABSPNB, FEP, GCR, (-) cyanosis, (-) edema GCS 15, oriented to 3 spheres, CNs intact

NE on ADMISSION

UPPER LIMB MOTOR FUNCTION

R LC5 5 5 Elbow flexorsC6 5 5 Wrist extensorsC7 5 5 Elbow extensorsC8 5 5 Finger flexorsT1 5 5 Finger abductors

NE on ADMISSION

LOWER LIMB MOTOR FUNCTION

R LL2 0 0 Hip flexorsL3 0 0 Knee extensorsL4 0 0 Ankle dorsiflexorsL5 0 0 Long toe extensorsS1 0 0 Ankle plantar flexorsS4-S5 (-) bowel incontinence

NE on ADMISSION

SENSORY FUNCTION: Light Touch

R LC2-T5 2 2T6-L2 1 1L3 0 1L4 0 0S4-S5 0 0

0 Absent1 Impaired2 Normal

NE on ADMISSION

SENSORY FUNCTION: Vibration

(+) vibration, UE(+) decreased, R ASIS(-) L ASIS

(-) bilateral patella

NE on ADMISSION

REFLEXES

R LBiceps 2+ 2+Triceps 2+ 2+Brachioradialis 2+ 2+Patellar 3+ 4+ (+) babinski,

BAnkle 4+ 4+ (+) clonus, B

LABS on ADMISSION

CBC: Hgb 114, Hct 0.349, WBC 8.8, Plt Ct 287, Neut% 0.890, Lymph 0.101%, Mono% 0.007, Eos% 0.000, Baso% 0.002

AFB SMEAR x 3: No acid fast bacilli seen

URINALYSIS: yellow, turbid, SG 1.030, pH 6.5, RBC 3/hpf ↑, WBC 7/hpf ↑, Bacteria 8,536/hpf ↑, few epithelial cells, no casts

LABS on ADMISSION

PT: 13 / 12.9 / 0.91 / INR 1.24

aPTT: 36.9 / 33.1

ECG: Sinus rhythm, normal axis

BLOOD CHEM: BUN 3.53, Crea 43, Na 141, K 3.9

URINE GS/CS: 100,000 colonies of E. coli

IMAGING

T1

T2

T3

T4

SUMMARY OF THE CASE• 21/F Nursing Student with a chief complaint of neck

pain and history of PTB exposure – 2-week history of progressive sensory deficit with deficit

starting T6 level– 1-week history of progressive motor deficit with deficit

starting L2 level– Associated with fever, malaise, easy fatigability, & urinary

and bowel changes; (-) weight loss, (-) anorexia– Normal pulmonary PE w/ (-) AFB smear; (-) cough– UMN signs: hyperreflexia with babinski and clonus– MRI showing compressive deformity of vertebra of T1-T2

level with soft tissue involvement

ASSESSMENT

Spinal Cord Compression, ASIA B, C7 last normal level, compression deformity T1-T2 level secondary to Pott’s disease

DISCUSSION: POTT DISEASE

POTT DISEASE

“…a tuberculous osteomyelitis of the spine that leads to compression of

vertebral bodies and a highly characteristic kyphotic deformity at

the thoracic or upper lumbar level ”

POTT PARAPLEGIA

“…pus or caseous granulation tissue may extrude from an infected

vertebra and gives rise to an epidural compression of the cord ”

PATHOPHYSIOLOGY

• Result of activation of tuberculosis at a site established by hematogenous spread.

• Infectious endarteritis causes bone necrosis and collapse of a thoracic or upper lumbar (less often cervical) vertebral body resulting in a highly characteristic angulated kyphotic deformity.

CLINICAL PRESENTATION• Slight compression/mild symptoms

pain in the back slight muscle weakness Tingling sensation other changes in sensation difficulty initiating and maintaining an erection (erectile

dysfunction, in men) Pain may radiate down a leg, sometimes to the foot exaggerated reflexes muscle spasms and increased sweating

CLINICAL PRESENTATION• Substantial compression/severe symptoms

block most nerve impulses severe muscle weakness, numbness paralysis and complete loss of sensation loss of bladder and bowel control A belt-like band of discomfort may be felt at the level of

spinal cord compression. Once compression begins to cause symptoms, damage

usually worsens from minimal to substantial unpredictably but rapidly in a few hours to a few days.

DISCUSSION: ASIA CLASSIFICATION

American Spinal Injury Association (ASIA) Classification

• A - "complete" spinal cord injury • no motor or sensory function is preserved in the sacral segments

S4-S5.

• B - "incomplete" spinal cord injury • sensory but not motor function is preserved below the

neurological level and includes the sacral segments S4-S5.

• C - "incomplete" spinal cord injury • motor function is preserved below the neurological level and more

than half of key muscles below the neurological level have a muscle grade of less than 3, which indicates active movement with full range of motion against gravity.

• D - "incomplete" spinal cord injury • motor function is preserved below the neurological

level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more.

• E - "normal"• it is possible to have spinal cord injury and neurological

deficits with completely normal motor and sensory scores.

DISCUSSION: CLINICAL SYNDROMES

Clinical Syndromes associated with incomplete spinal cord injuries

• Central cord syndrome – associated with greater loss of upper limb function compared to

lower limbs• Brown-Séquard syndrome

– injury to one side with the spinal cord, causing weakness and loss of proprioception on the side of the injury and loss of pain and thermal sensation of the other side

• Anterior cord syndrome – injury to the anterior part of the spinal cord, causing weakness

and loss of pain and thermal sensations below the injury site but preservation of proprioception that is usually carried in the posterior part of the spinal cord.

• Tabes Dorsalis – injury to the posterior part of the spinal cord,

usually from infection diseases such as syphilis, causing loss of touch and proprioceptive sensation.

• Conus medullaris syndrome – injury to the tip of the spinal cord, located at L1

vertebra.• Cauda equina syndrome – injury to the spinal roots below the L1 vertebra.

DISCUSSION: IMAGING & DIAGNOSIS

Radiologic Findings• Lytic destruction of anterior portion of vertebral

body• Increased anterior wedging• Collapse of vertebral body• Reactive sclerosis on a progressive lytic process• Enlarged psoas shadow with or without

calcification• Intervertebral disk spaces are decreased or

obliterated• Fusiform paravertebral shadows suggest abscess

formation

Collapsed T9-11 and anterior wedging

Day 0 – narrowed intervertebral disk space, hazy vertebral body edges

Day 14 – collapse of vertebral bodies

• Vertebral collapse, sever anterior wedging

MRI

Bilateral psoas abscesses are frequent complication in lumbar involvement

Axial T2 demonstrate marrow edema at L2-L4. Right paraspinal rim enhancing fluid is demonstrated compatible with a paraspinal abscess.

DIAGNOSIS

• The diagnosis still depends on biopsy for culture and pathologic examination of the affected tissue because radiographs are not diagnostic.

• Imaging modalities such as CT or MRI however help target the biopsy site.

• It is mentioned that MRI is the modality of choice because it can discriminate between abscess and granulation tissue and can delineate soft tissue masses and identify the amount of bone destruction.

DISCUSSION: TREATMENT

TREATMENT: ANTI-KOCH’SSITE DURATION RATINGLymph node 6 Level 1Bone and joint 6-9 Level 1Pleural disease 6 Level 2Pericarditis 6 Level 2CNS 9-12 Level 3Disseminated 6 Level 2Genitourinary 6 Level 2Abdominal 6 Level 1

TREATMENT: ADJUNCTIVESITE CORTICOSTEROIDS RATINGLymph node NOT RECOMMENDED Level 3Bone and joint NOT RECOMMENDED Level 3Pleural disease NOT RECOMMENDED Level 1Pericarditis RECOMMENDED Level 2CNS STRONGLY REC. Level 1Disseminated NOT RECOMMENDED Level 3Genitourinary NOT RECOMMENDED Level 3Abdominal NOT RECOMMENDED Level 3

TREATMENT: SURGERYSurgery in addition to chemotherapy is indicated in the following situations (Parthasarathy et al):1. Those less than 25 years of age, in whom the initial angle

of kyphosis is more than 30°2. Those who develop progressive kyphosis while on

ambulant chemotherapy3. Children aged less than 10 years with destruction of the

vertebral bodies who have partial or no fusion during the adolescent growth spurt

4. Those with compression of the spinal cord whose neurological status deteriorates in spite of chemotherapy

DISCUSSION: ADDF

Anterior Decompression and Fusion of the Spine

• A major surgery which utilizes a skin incision over the front of the body to approach the spine

• simple, requires less operative time, and provides excellent exposure up to the level of T2.

• There was no long-term morbidity attributed to the approach and procedure (according to study by MM. Prabhakar)

Indications• Degenerative conditions causing compression of spinal

cord or spinal nerves, e.g. intervertebral disc prolapse, posterior vertebral body osteophytes

• Instability of the spine• Spine fracture• Spinal tumour• Spinal infection (usually tuberculous or bacterial)• Spinal deformity• Miscellaneous conditions causing spinal cord or spinal

nerve damage

Fig 1: Titanium plate and screw device secured to the vertebral bodies

underlying musculature dissected to expose anterior cervical spine

esophagus and trachea retracted midline, carotid artery and associated structures laterally

The sternal-splitting approach from C4-T4

In the study.. Anterior Decompression for Cervicothoracic Pathology: A Study of 14 Patients MM Prabhakar, MS1,2 and Tejas Thakker, MS2

Method: left oblique incision along the medial border of the sternocleidomastoid muscle to the sternal notch. The platysma was incised, and the plane between the carotid and tracheoesophageal sheaths separated using the finger. The anterior aspect of the low cervical spine was exposed after retracting the tracheoesophageal sheath laterally. The strap muscles were detached at their origins. The lateral margin of dissection extended to the longus colli muscle on either side. Using metal markers, a radiograph was taken to confirm the target level. Using this low cervical approach, exposure to the T2-T3 level obtained.

Sequential Surgical ProcedureRetractors placed to protect the soft tissues of the neck

intervertebral discs are removed at the level(s) to be decompressed

If multiple levels are to be decompressed, surgeon may remove the vertebral bodies between the evacuated disc spaces ---'corpectomy'.

Sequential Surgical Procedure

“Interbody grafts” - inserting bone grafts within each disc space to have a living bridge of bone between the previously distinct vertebrae “a spine fusion “

Sequential Surgical Procedure(2) banked human cadaver bone (allograft), or

(3) synthetic scaffold into which bone graft may be inserted (metal or carbon fiber cages)

Sequential Surgical Procedure

—for further stability, promoting adequate fusion. preventing dislodgement of bone graft

Sequential Surgical Procedure

Recovery—1-4 days in hospital **Failure of bone graft healing is among the principal reasons for repeat surgery in these cases

(A) Radiograph showing tuberculosis of C7 with prevertebral abscess. (B) Eighteen-month postoperative (C7 corpectomy and fusion) radiograph showing solid bony fusion from C6 to T1

(A) Tuberculosis of T2 with epidural abscess. (B) Postoperative view after anterior curettage with fusion and posterior Hartshill fixation. (C) Postoperative clinical picture

Source: Anterior Decompression for Cervicothoracic Pathology: A Study of 14 Patients MM Prabhakar, MS1,2 and Tejas Thakker, MS2

Accepted January 2006.

Source: Anterior Decompression for Cervicothoracic Pathology: A Study of 14 Patients MM Prabhakar, MS1,2 and Tejas Thakker, MS2

Accepted January 2006.

Tuberculosis of T2 with abscess (A) and picture (B and C) showing postoperative CT scan illustrating the position of the iliac crest graft in the decompressed space.

Risk Factors in Bone Graft Failure

increasing numbers of levels

to be fused

smoking or other sources of

nicotine

non-compliance with activity restriction and/or brace wear

poor bone quality

(osteoporosis)

POST-OP FINDINGS

POST-OP PE

Stretcher-borne, awake, coherent, NICRDBP 100/60 HR 72 RR 20 Temp afebrileAS, PC, (-) CLAD, (-) NVE, (-) ANMECE, CBS, (-) r/wAP, DHS, NRRR, (-) murmurSoft, flabby, nontender abdomen, NABSPNB, FEP, GCR, (-) cyanosis, (-) edema GCS 15, oriented to 3 spheres, CNs intact

POST-OP NE

LOWER LIMB MOTOR FUNCTION

R LL2 2 2 Hip flexorsL3 2 2 Knee extensorsL4 2 2 Ankle dorsiflexorsL5 2 2 Long toe extensorsS1 2 2 Ankle plantar flexorsS4-S5 (+) anal wink, good sphincter tone

POST-OP NE

SENSORY FUNCTION: Light Touch

R LC2-T5 2 2T6-L2 2 2L3 2 2L4 2 2S4-S5 2 2

0 Absent1 Impaired2 Normal

POST-OP NE

REFLEXES

R LBiceps 2+ 2+Triceps 2+ 2+Brachioradialis 2+ 2+Patellar 2+ 2+ (-) babinskiAnkle 2+ 2+ (-) clonus

THANK YOU!