· First, observe the patient. If the patient lies in a natural position such as sleep, then coma is likely not extremely deep. Automatisms such as coughing or swallowing have little significance.

· Assess level of unconsciousness, looking for response to voice (call out name loudly) as well as to peripheral (nail bed pressure for example) and central stimulation with noxious (cotton tip in nostril, supraorbital pressure, trapezius pinch, sternal rub) stimuli.

2. Cranial nerves:

· Evaluate pupil reactivity, eye movement (spontaneous, roving conjugate or dysconjugate, none), blink to threat in each eye (visual fields), and fundoscopic exam (papilledema or hemorrhage).

· Assess corneal reflex using cotton tip on cornea (not sclera), usual response is blink.

· Assess gag reflex either with a tongue depressor or by suctioning the patient on the ventilator.

· Assess doll's eye (oculocephalic) response, normal response in unconscious patient is for eyes to remain or quickly return to and cross midline as head is turned.

· Assess oculovestibular response (cold calorics) by first using otoscope to make sure external ear canals patent without tympanic membrane rupture. Then instill 30 cc of cold water into each canal with patient positioned at 30 degrees. Repeat in opposite canal after 5 minutes. Normal response with cold water is nystagmus with the fast phase away from the tested ear.

· Observe respiratory pattern as well as if patient is overbreathing the ventilator. Respiratory pattern can be helpful in localizing lesion within brain stem.

3. Motor:

· Scoring system for conscious and unconscious patients (out of 5): 0 = no movement, 1 = flicker of a movement, 2 = movement in absence of gravity, 3 = movement against gravity, not against resistance, 4 = partial movement against resistance, 5 = full movement against resistance.

· Assess spontaneous or purposeful movements through observation.

· Assess response to noxious stimuli with peripheral stimulation (nail bed) in each extremity. Document response: localization to pain, withdrawal to pain, flexor or extensor posturing, etc.

4. Sensory:

· If spinal cord injury suspected, look for level on trunk; otherwise simply evaluate response to pain in all four extremities and gauge response.

5. Reflexes:

· Always test biceps, triceps, brachoradialis, patellae, ankle jerks, and plantar responses (Babinski).

· In coma patients, look for asymmetry.

· Note that a variety of metabolic processes can cause babinski response bilaterally.

Plum F, Posner JB. The Diagnosis of Stupor and Coma Edition 3. FA Davis Company: Philadelphia. 1982.

PROGNOSIS IN HYPOXIC/ISCHEMIC COMA

1. General considerations: prognosis is guided by the largest, but still relatively small, study in which coma outcomes are stratified based on coma exams at various time points (see reference below). No definitive data as to long-term outcome exists, but this study can guide prognosis discussions with families.

2. The initial exam is key and therefore documenting pupils, etc. on initial exam is extremely important when evaluating the patient:

3. Poor prognostic signs: if the following are present, there is virtually no chance of regaining meaningful recovery:

· On initial exam: no pupillary light reflex.

· On day one (24 hours out):

- Motor exam with only flexor or extensor posturing or no movement at all (i.e. the patient does not obey commands or does not localize or withdraw to peripheral painful stimuli) and

- Eye movement roving/dysconjugate or not moving at all.

· On day three (72 hours out): motor exam with only flexor or extensor posturing or no movement.

· At one week:

- Motor exam anything less than obeying commands and

- Three day eye opening was not spontaneous and

- Initial exam spontaneous eye movements were neither orienting nor roving conjugate.

Levy DE, Caronna JJ, Singer BH, Lapinski RH, Frydman H, Plum F. Predicting outcome from hypoxic-ischemic coma. JAMA. 1985 Mar 8;253(10):1420-6.

BRAIN DEATH

1. State laws vary, but a patient is generally considered expired when there is no brain stem function.

2. Brain death cannot be declared if the patient is hypothermic (T < 32.2°C). If they are intoxicated or have ingested a substance, they cannot be declared dead until 4-5 half lives of the suspected substance have passed. Note that substances we give patients such as paralytics, benzos, sedatives, etc. also fall under this category.

3. General criteria: at least 24 hours must pass between consecutive examinations. Patient should have fixed pupils without eye movements, and should not have any of the following reflexes: corneals, gag, oculocephalic, oculovesibular (cold calorics), or overbreathing the ventilator.

4. Confirmatory tests can be helpful and are required by law in some states. They include any of the following:

· An isoelectric EEG for 30 minutes with the machine set at high gain.

· No cerebral blood flow as determined by radionucleotide angiography.

· A “positive” apnea test (generally has less false positive results and is therefore used most often clinically).

5. Do not forget that these patients are ideal candidates for organ donation, and consult the family and your local donor network accordingly.

Wijdicks EF. The diagnosis of brain death. N Engl J Med. 2001 Apr 19;344(16):1215-21.

MINI MENTAL STATUS EXAM (MMSE)

Category	Question	Score
Orientation	Name the day/date/month/season/year	5
Orientation	Name the floor/hospital/town/state/country	5
Registration	Name three objects and have patient repeat them immediately	3
Attention	Serial 7's or spell "world" backwards or days of week backwards	5
Recall	Ask the patient to name three objects stated above after 3 minutes	3
Language and Praxis	Point to a pencil and watch and ask the patient to name them	2
	Ask patient to repeat the following: "No ifs, ands, or buts"	1
	Follow a three stage command: "Take a paper in your right hand, fold it in half, and put it on the floor"	3
	Read and obey the following sign: "Close your eyes"	1
	Write a sentence	1
	Copy this design: intersecting pentagons	1
Total		30

CLOSE YOUR EYES

Folstein MF, Folstein SE, McHugh PR. "Mini-mental state". A practical method for grading the cognitive state of

patients for the clinician. J Psychiatr Res. 1975 Nov;12(3):189-98.

GLASGOW COMA SCALE

Total score is the sum of eye + verbal + motor. The range of scores is from 3 (totally unresponsive) to 15 (normal). Intubated patients cannot have verbal responses, so they are scored as the sum of eye + motor, followed by a T and the maximum score is thus 10T.

Eye opening

Score

Verbal response

Score

Motor response

Score

spontaneous

to voice

to painful stimuli

never

oriented

confused

inappropriate words

unintelligible sounds

none

follows commands

localizes pain

withdraws from pain

flexor response

extensor response

none

PERIPHERAL NEUROPATHY

1. Causes:

Acute inflammatory process: Guillan-Barré syndrome, critical illness, diphtheria, shellfish toxin
Metabolic: diabetes mellitus, uremia, liver disease, B12 or folate deficiency
Infectious/granulomatous: HIV/AIDS, leprosy, sarcoid
Vasculitis: lupus, polyarteritis nodosa, rheumatoid arthritis
Neoplastic/paraneoplastic
Toxin: EtOH, drugs, metals (such as arsenic and thallium)
Hereditary
Entrapment

2. Identify nerve distributions of motor/sensory disturbances (symmetric? distal vs. proximal?), reflexes, autonomic symptoms, time course, and onset age. Note that Guillan-Barré syndrome presents with sudden ascending weakness and hypo- or areflexia beginning at the ankles.

3. Diagnosis: consider CBC, ESR, chem 7, HbA₁c, TSH, B12, LFTs, TSH, RPR (treponemal antibody test if syphilis is truly suspected), CXR, 24 hour urine for heavy metals, SPEP/UPEP, rheumatoid factor, and ANA. EMG is helpful in most patients; consider nerve conduction studies. In selected cases, a lumbar puncture may be helpful in looking for protein and/or signs of inflammation.

Hughes RA. Peripheral neuropathy. BMJ. 2002 Feb 23;324(7335):466-9.

SEIZURES

1. If patient is still seizing—remember your ABC's:

· Give O₂ by face mask, position patient on side to prevent aspiration. Suction airway as needed. Do not try to insert airway.

· Prevent patient from injuring himself/herself.

· If seizures continue after 2-3 minutes, try to start an IV and abort the seizure with Ativan 2 mg. Alternatively, Ativan IM q5 minutes to maximum of 8 mg or Valium PR 20 mg.

· Give thiamine 100 mg IV first, then 1 amp D₅₀ IV.

· If the seizure has been going on for longer than 10 minutes or is not easily responsive to benzodiazepines, the patient is likely in status epilepticus and the patient will need ICU management.

· Only if an absolute certain diagnosis of severe hyponatremia is established should treatments such as iso- or hypertonic saline be used to halt a seizure.

2. Once seizure is stopped:

· Place oral airway. Get ABG if patient appears cyanotic.

· Establish IV access and send basic labs (CBC with differential, electrolytes, BUN, creatinine, glucose, Ca, Mg, albumin, antiepileptic levels).

· Evaluate if this is status: continuing seizing for > 30 minutes, no consciousness after 30 minutes, if patient seizes again without achieving normal consciousness. If the patient is in status epilepticus, send the patient to the ICU and consult neurology.

3. Load with phenytoin 20 mg/kg in 3 divided doses at 50 mg/min (usually 1 g total); alternatively, always use fosphenytoin when available at the same dose as its load is better tolerated.

·Remember, phenytoin (but not fosphenytoin) is not compatible with glucose-containing solutions or with Valium. If you have given these meds earlier, you need a second IV.

4. Consider common causes of seizures (i.e. basic labs and a head CT for new onset seizures):

· Alcohol withdrawal (2 mg ativan IV post-seizure may help to prevent recurrence).

· CNS lesion including infections (tumor, CVA, head injury, meningitis/encephalitis, etc.).

· Meds (demerol, benzo withdrawal, penicillin, lidocaine toxicity, INH [only stops after giving Vitamin B6), ASA, TCA, cocaine, Benadryl, amphotericin, theophylline, buproprion/Zyban etc.).

· Metabolic (low glucose, Na, Ca, or Mg).

· Toxins (CO, heavy metals, many drugs of abuse or withdrawal from these drugs).

· Other (HIV, malignant hypertension, hypoxia, uremia).

5. Write for seizure precautions. Watch for metabolic acidosis and rhabdomyolysis.

6. Remember that all patients with medical conditions which could potentially affect their ability to safely operate a motor vehicle (i.e. seizures, syncope) must be reported to the local department of motor vehicles by the physician (this means you).

Lowenstein DH, Alldredge BK. Status epilepticus. N Engl J Med. 1998 Apr 2;338(14):970-6.

MANAGEMENT OF STATUS EPILEPTICUS

1. Initial management:

Assess and manage airway
Place on continuous cardiac monitoring and pulse oximetry
Check fingerstick glucose and correct
Obtain IV access and give fluids.
Give thiamine 100 mg IV and dextrose (50 cc D₅₀ IV push).

2. Start anti-convulsant therapy:

Start with lorazepam 0.1 mg/kg IV at 2 mg/minute.
If seizures continue for > 2-3 minutes after lorazepam given, load with phenytoin 20 mg/kg IV at 50 mg/min or fosphenytoin 20 mg/kg PE IV at 150 mg/min).

3. Look for causes of seizure:

· Take a focused history and examine the patient.

· Look for history of seizure disorder or other illness, trauma, focal neurologic signs, signs of medical illness such as infection, liver disease, renal disease, substance abuse.

· Check CBC, electrolytes, calcium, ABG, liver function tests, BUN, creatinine, toxicology, serum anti-epileptic drug levels.

· If patient stable, obtain head CT to rule out bleed or mass.

4. Anti-convulsant therapy for refractory seizures:

If seizures continue for > 30 minutes after phenytoin or fosphenytoin load:

- Intubate the patient

- Administer additional 5-10 mg/kg phenytoin or fosphenytoin

If seizures continue for > 40 minutes, give phenobarbital 20 mg/kg IV at 50-75 mg/minute and if seizures continue, can give additional 5-10 mg/kg.
If seizures continue after all of the above and the patient has been in status for > 1 hour, proceed to anesthesia with midazolam or propofol.

Lowenstein DH, Alldredge BK. Status epilepticus. N Engl J Med. 1998 Apr 2;338(14):970-6.

ACUTE ISCHEMIC STROKE

1. Initial evaluation:

· Suspect stroke whenever a patient has sudden onset of neurologic signs such as hemiparesis, aphasia, hemianopia, or AMS.

· Begin assessment with the "ABC's" of resuscitation.

· Classify stroke early: the key to early diagnosis and treatment of stroke is the emergent non-contrast head CT, confirming the absence or presence of hemorrhage.

· All patients should get EKG, CXR, and consideration for rule out MI (association with heart disease).

2. Acute treatment for stroke:

· Thrombolysis: see below.

· Consider intraarterial thrombolytic therapy in occlusion of MCA.

· BP control: only if SBP > 200 mmHg or MAP > 130 mmHg or concomitant aortic dissection, acute MI, CHF, ARF, hypertensive encephalopathy, or those receiving TPA. Lower slowly and avoid more than a 20 mmHg reduction. Use B-blockers or ACE inhibitors preferentially; CCBs, nitrates, and hydralazine should be avoided. Remember Cerebral perfusion pressure (CPP) = MAP – intracranial pressure (ICP). Lowering MAP can decrease CPP; hence, permissive hypertension.

· Glucose control: hyperglycemia is an independent risk factor for poor outcome. Aim for < 170 mg/dl.

· Vomiting: common in stroke, especially if vertebrobasilar or hemmorrhagic. Control of secretions using NGT, frequent suctioning important given dysphagia.

· Dysphagia: keep patients NPO until formally evaluated by speech, given their high aspiration risk.

· IV fluids: mild restriction is recommended; avoid hypo-osmolar fluids such as D₅W due to worsening of cerebral edema.

· Anticoagulation: IV heparin has uncertain usefulness and is controversial even among neurologists. Most would agree on at least two situations of evidence-driven use: ischemic stroke during episode of afib or known intra-cardiac thrombus on echo. If used, avoid boluses. Most stroke patients should be on DVT prophylaxis.

· Aspirin: Benefit towards combined endpoint of death or non-fatal stroke. Treat initially with 160-325 mg QD. Also beneficial for secondary stroke prevention; can use low dose (e.g. 81 mg QD) to prevent bleeding complications. In some circumstances, such as a patient with a stroke already on ASA, addition of clopidogrel (Plavix®) may be useful.

· Frequent neurological checks to monitor progression of neurologic signs and symptoms.

3. Thrombolysis: current guidelines for using TPA

· Ischemic, hemispheric strokes only (no hemorrhagic strokes!)

· Less than 3 hours from onset of symptoms, age 18-80. Note that if patient awakens with symptoms or cannot give accurate time of stroke onset, the time begins when patient was last asymptomatic.

· Symptoms are moderate-severe and not improving (avoid if in stupor or coma).

· Avoid in people with bleeding risks, recent surgery, recent stroke, recent seizures, sustained BP > 185/110 (if brought down to this level with labetolol, etc. may still qualify for lysis).

· Make sure patient has no contraindications to t-PA.

· Significant risk of hemorrhagic transformation so strict adherence to protocols and inclusion/ exclusion criteria is essential.

4. Hospital care:

Consider adjunctive testing early: MRI, MRA, carotid dopplers, echo with bubble study.
Half of the deaths due to stroke are secondary to medical complications.
Investigate fever early and promptly give anti-pyretics.
Patients. with cardiac disease should be on telemetry with frequent assessments.
Seizures may occur in 5% or more of patients with ischemic stroke. If seizures occur, give anticonvulsants.
Prevention of DVT, PE, pneumonia, UTI, decubitus ulcers.
Mobilization early 24-48 hours after completion of stroke, even passively, helps prevent contractures.

5. Cerebral edema and elevated ICP:

· Look for signs: decreased level of consciousness, loss of spontaneous venous pulsations on fundoscopic exam, blown pupil on ipsilateral side of stroke, progression of focal neuro deficit, corticospinal signs (weakness, hyperreflexia).

· If suspected ® urgent head CT (in patients at high risk, remember that radiological signs may appear prior to clinical signs; therefore, serial CT scans may be necessary). Time to call neuro.

· Treatment:

- Elevate head of bed to 30 degrees.

- Mannitol: 25-50 g IV q 3-5 hours (max of 2 g/kg qd) for osmotic diuresis, follow serum osmolality.

- Furosemide: 20-80 mg IV q 4-12 hrs can be used to supplement diuretic effect of mannitol.

- Replacement fluids can be given to maintain calc. serum osmolality of 300-320 mOsm/kg

- Glucocorticoids are not recommended and may be harmful.

- Intubation and hyperventilation to achieve pCO₂ of 25 – 30 mmHg if necessary.

- Call neurosurgery for possible life-saving decompression and/or invasive ICP monitoring.

Brott T, Bogousslavsky J. Treatment of acute ischemic stroke. N Engl J Med. 2000 Sep 7;343(10):710-22.

SUBARACHNOID HEMMORRHAGE (SAH)

Most commonly the result of ruptured aneurysm or AVM, associated with many conditions such as Marfan’s, Ehlers-Danlos syndrome, polycystic kidney disease.

1. Symptoms: classically described as the worst headache of the patient’s life, often during exertional activities including sex. Examination can be benign early and therefore this classic history prompts quick evaluation for SAH.

2. Exam: look for signs of meningeal irritation. Blood is a pyretic and low-grade fever can be common. A full neuro exam looking for focal deficits as well as signs of increased ICP is a must. On fundoscopic exam, can occasionally see subhyaloid hemorrhages.

3. Diagnosis: non-contrast head CT is the test of choice, but can miss 5-10% of cases. If a CT is non-diagnostic but suspicion still exists, a lumbar puncture must be performed. RBCs should clear from tube 1 to 4 if traumatic tap but will be relatively stable if the patient has SAH. Xanthrochromia can be seen after blood is in the CSF for more than 6 hours. If either CT or LP indicates SAH, call neurosurgery early for management and decisions on treatment, angiography, etc.

4. Treatment: consult neurology and neurosurgery early. Preoperatively, prevention of vasospasm as well as recurrent hemorrhage is the goal. Control BP, minimize patient straining and excitement with stool softeners as well as possible sedation. Most management should be deferred to these other services.

Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. 2000 Jan 6;342(1):29-36.

ALTERED MENTAL STATUS (AMS)

1. If the patient has AIDS, see Infectious diseases: HIV and altered mental status.

2. Differential diagnosis:

· Metabolic – B₁₂, thiamine deficiency, hepatic encephalopathy (rarely, Wilson’s disease, niacin deficiency).

· Oxygen – hypoxemia is a common cause of confusion. Also, hypercarbia, anemia, decreased cerebral blood flow (e.g., from low cardiac output), sepsis, and carbon monoxide poisoning.

· Vascular – Stroke (carotid, MCA, ACA, vertebrobasilar, hyperviscosity, hypertensive encephalopathy), hemorrhage (ICH, subarachnoid, subdural, epidural), vasculitis, TTP, DIC

· Endocrine – hyper/hypoglycemia (can cause focal signs), hyper/hypothyroidism, high/low cortisol. Electrolytes –low sodium, hyper/hypocalcemia, hypermag, hypophos, abnormal LFTs

· Seizures – post–ictal (confusion), status epilepticus (nonconvulsive), complex partial seizures Structural – lesions with mass effect, hydrocephalus

· Tumor, Trauma, or Temperature (either fever or hypothermia)

· Uremia – also dialysis desequilibrium syndrome. A related disorder is hepatic encephalopathy.

· Psychiatric –dx of exclusion. ICU psychosis and “sundowning” are common. Rarely, Porphyria.

· Infection – any sort, including CNS, sepsis. A simple UTI in an elderly patient can bring out signs of an old, focal stroke.

· Drugs –intoxication or withdrawal from alcohol, illicit, prescribed drugs, OTC, other (antichol, etc). Degenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s cause a slower decline in cognitive function.

3. Initial Evaluation of AMS:

· A standard approach: use the “DON’T” pneumonic

- Dextrose, 1 amp of D₅₀ after thiamine, usually after fingerstick

- Oxygen by nasal cannula or mask, with oropharyngeal airway if necessary

- Naloxone (Narcan®), usually 0.4-1.2 mg IV if there is even a remote possibility of opiate OD

- Thiamine, 100 mg IV (before glucose to prevent precipitation of Wernicke's)

· Neuro exam: See Neurology: Examination of the comatose patient.

· Key symptoms to focus on: fever, tachycardia, O₂ saturation, myclonus (uremia, cerebral hypoxia, hyperosmolar non-ketotic coma), tremor (withdrawal, autonomic symptoms, hyperactive), asterixis (liver/renal failure, pulm encephalopathy, drug intoxication). All suggest metabolic rather than structural disease as etiology.

· Labs: CBC, chem 7, LFTs, Ca/Mg/Phos, Utox, U/A, ABG, ECG, blood and urine cultures, CXR. NH₄is can be used as an initial confirmatory test for hepatic encephalopathy, but does not rule out other causes and cannot be followed over time. CSF glutamine, if available, is a better for hepatic encephalopathy.

· Have a low threshold for getting a non-contrast head CT in any patient with focal neurologic signs or at risk for CVA. In general, it is much easier to obtain a head CT from the emergency department than from the floor once the patient is admitted. If you think patient is herniating (blown pupil), call neurosurgery and consider dexamethasone, hyperventilation, and mannitol.

· The old truism about lumbar punctures applies here: if you think about it, you should probably do it—particularly in any patient with fever or meningeal signs, or any patient who is immunosuppressed. (see Infectious diseases: Meningitis and Procedures: Lumbar puncture for more details).

HEADACHE

1. New = potentially worrisome:

Temporal arteritis: the danger is visual blindness due to ophthalmic artery occlusion in untreated patients. Age >50, 85% headache, 70% temporal artery tenderness, 65% jaw claudication. Diagnosis – 95% ESR > 50, biopsy of temporal arteries. Pathology – need serial sections for maximum yield. Treatment is immediate high-dose prednisone (60-80 mg/day) for 1-2 years. See also Rheumatology: Temporal (giant cell) arteritis.
Tumor: severity not predictive, worse when lying or head lowered, awakens patient from sleep. Diagnosis – MRI is best.
Subarachnoid hemorrhage (see also Neurology: Subarachnoid hemorrhage): Sudden/explosive, stiff neck, worst headache of life. If known SAH patient suddenly worse, think obstructive hydrocephalus: intubate, mannitol, head of bed up, call neurosurgery.
Meningitis: fever, neck pain/stiffness, photophobia. Diagnosis via LP, nice to have head CT to rule out significantly increased ICP. Should start antibiotics immediately, as have 6 hours before spinal fluid is sterilized. See also Infectious diseases: meningitis.

2. Old = likely benign if unchanged:

· Migraine: visual changes that often move such as jagged lines, white spots, geometric shapes photophobia, nausea/vomiting. Hemicranial in location, sleep helps, and there is often a positive family history. Migraines usually last hours to days. 73% of patients have their first attack by age 30. There is a diurnal variation (most occur within 6 hours of a certain time). Diagnosis: identify triggers (stress, menses, OCPs, fatigue, chocolate, alcohol, caffeine). Treatment: abortive (parental most effective; NSAIDs, sumitriptan, ergots) vs. prophylactic (beta-blockers, TCA, CCBs, anticonvulsants).

· Cluster: usually occurs in males age 20-50 years old. Headache is unilateral, peri/retroorbital, severe, and has a circadian pattern. It occurs 1-3x/day lasting hours, is associated with ipsilateral autonomic symptoms, and 50% have alcohol sensitivity during the attack. Abortive therapy: 6L oxygen x15 minutes, sumitriptan, or prednisone burst (try to avoid). Prophylactic treatment: calcium channel blockers, ergots, lithium.

· Trigeminal neuralgia: electric, shock-like volleys of pain in V2/V3>>>V1 distribution; unilateral, has trigger sites, and lasts seconds. Treatment: anticonvulsants (start with carbamazepine as little as 200 mg/day), lithium; if this fails, consider surgical decompression or radiofrequency ablation of the nerve.

LOW BACK PAIN

1. Red flags: fever, weight loss, night sweats, worse at rest or at night, duration > 1 month, history of cancer, history of chronic infection, age > 50, history of IVDU, steroid use, neurologic deficit, percussion tenderness of spine or costovertebral angle, abdominal/rectal/pelvic mass, straight leg sign (sciatic nerve, L5, S1), reverse straight leg raise sign (L2, L3, L4, femoral nerve).

2. Standard Approach to low back pain:

If no serious risk factors and < 1 month duration: symptomatic treatment for two weeks; if persists, then reconsider other options.
If serious risk factors or > 1 month duration: consider CBC, ESR, U/A, CXR, skin exam, imaging, specialist consultation, other lab tests.
If rapidly progressive neurologic deficit: immediately consult by neurology or neurosurgery.

3. Vertebral osteomyelitis/discitis versus epidural abscess: neither is ruled out by the absence of systemic symptoms or neurologic deficits, but usually present with back pain and point tenderness. ESR is usually > 30-40. Blood cultures are only 30% sensitive. Both usually arise from hematogenous seeding, and you must look for the source. Both are better diagnosed by MRI with contrast (95% sensitive at 1-2 weeks, and 99% sensitive thereafter) than CT. A lumbar puncture is not appropriate. For osteomyelitis, a CT-guided needle biopsy is necessary. Osteomyelitis requires IV antibiotics; epidural abscess often also requires surgical intervention. Follow-up scan not needed until 6weeks.

4. Nerve root patterns:

L4: quad reflex; medial calf sensation; quadriceps, thigh adductors, tibialis anterior motor; (+) reverse straight leg raise test.
L5: no reflex; foot dorsum/lateral calf sensation; foot eversion, tib anterior, hip abduction, toe dorsiflexion motor; (+) straight leg raise test.
S1: ankle reflex, foot plantar/lateral foot sensation; foot plantar, toe flexors, hip extensors motor; (+) straight leg raise test.

CORD COMPRESSION

1. Suspect this diagnosis in patients with:

· New weakness or change in sensation (especially if they have a demonstrable level)

· New bowel/bladder retention or incontinence (however, constipation is not relevant)

2. Prognosis is dismal for patients with no function for > 24 hours. Prognosis is best for patients with new, incomplete loss (i.e. weakness).

3. This is a surgical disease—call neurosurgery early. That having been said:

· Stabilize the spine: collars for C-spine, "turtle shells" (TLSO) for T/L-spine.

· Dexamethasone (10 mg load and then 6 mg q 4 hours or 4 mg q 6 hours)—not always indicated (in case of traumatic fracture for instance).

· If tumor, proceed to radiotherapy.

5150

For those of you unfamiliar with Van Halen, this is an involuntary hold for 72 hours for one of the following three reasons:

1. Danger to self

2. Danger to others

3. Grave disability (unable to provide food, clothing, shelter).

Usually done by police or psychiatrists (mental health professionals), not internists. Good for 72 hours.

5250

Involuntary hold for 14 days. Usually pursued after 5150 if the patient is still unable to make decisions for self. Requires hearing with judge, and same 3 criteria need to be met.