Case Based for September

Case: 44-year-old female with “worst headache” of her life

DX: SAH

44-year-old white female, right-handed, presented on a Tuesday before shift change at 6:45 PM with the worse headache of her life. She was signing in at the kiosk with her 7 y.o son, and she just slumped down onto the floor, started having mild convulsions.  Further history from a friend who came in later, related that she has history of chronic alcohol abuse and had been on a “Daniel Fast” subsisting on nuts, vegetables and water, avoiding meat for the past week. She told her friend that she was trying to wean herself off the alcohol, although seen at a party 2 days ago with a cocktail in her hand.

Vital signs showed elevated BP at 206/114, afebrile, sats at 99% on RA and HR in the 60s. She became unresponsive after the convulsions. No meningeal s/sx, no rash, was ambulatory prior to the seizure, normocephalic, no head trauma noted on exam. Pupils, equal at 4 mm, sluggishly reactive. Rest of her physical exam was unremarkable.

Review of her medications included alprazolam and citalopram for anxiety disorder. She worked as an occupational therapist.

She was rushed in for a CT of the head and initially given lorazepam 2 mg IV,   Keppra 1 gm IV.  Radiological imaging of her head showed moderate volume of bilateral acute SAH more pronounced on the right, mass effect on the R hemisphere, effacement of the R lateral ventricle with 5 mm right to left midline shift. No skull fracture noted. Portable chest Xray was unremarkable.

She was subsequently intubated successfully with a GCS of 4 under RSI, given midazolam 2 mg IV, rocuronium 75 mg IV; verified ETT placement with capnometry and a repeat chest radiograph.

Subsequent lab tests showed WBC 12.4, Hgb 9.5, Hct 29.7% and platelets adequate at 362K. Except for a serum K of 3.1, CMP was unremarkable, with a Mg of 1.9, total bilirubin 0.5. Rest of her LFTS were all WNL.

Differential DX: seizures from Delirium tremens, SOL brain, IC Hge, ruptured aneurysm, SAH, Alcoholic encephalopathy

 

SUBARACHNOID HEMORRHAGE:  Intracranial bleeding within the subarachnoid space, between the arachnoid and pia matter overlying the brain.

The classic presentation of aneurysmal SAH is a SUDDEN-ONSET, SEVERE HEADACHE TYPICALLY DESCRIBED AS THE “WORST HEADACHE OF MY LIFE”. Every patient with this kind  of headache, often referred to as a “thunderclap headache” should be evaluated for SAH.

Most patients are neurologically intact with a severe onset of headache peaking within 1 hour.  Three large studies involving 5,283 patients presenting with severe headache, 329 or 6% were diagnosed with SAH. Location of the headache is not usually useful, can be localized or generalized, but qualitatively different, described as more severe.

Associated symptoms of SAH include vomiting, neck pain or stiffness, loss of consciousness. They may also have preceding meningismus  with subsequent lower back pain for several hours after the bleeding is noted, due to the breakdown of blood products into the spinal canal, leading to aseptic meningitis. They may present with altered mental status, yet coma is unusual.  Seizures is noted during the first 24 hours in less than 10%, and is indicative of a poor prognosis.  Mortality rate from SAH is noted to be 22%.

Prodromal symptoms of a SENTINEL HEADACHE that precede a major SAH, may occur days to weeks prior to aneurysm rupture. Such sentinel headache may represent either a minor hemorrhage/”warning leak” from an acute dissection, thrombosis or expansion of the cerebral aneurysm.

While the onset of symptoms in the setting of physical exertion, activities associated with Valsalva maneuver, emotional stress suggest SAH,  aneurysmal SAH occurs most often during nonstrenuous activity, during rest or sleep.

Notable physical exam findings include hypertension and meningismus.  TERSON syndrome with preretinal hemorrhages may be seen and imply a poorer prognosis, indicative of a more abrupt increase in intracranial pressure. Nearly any neurologic sign may be present and will depend on the location the hemorrhage, presence or absence of hydrocephalus, elevated intracranial pressure, ischemia, infarction, or hematoma.  Using the HUNT and HESS grading system for SAH, coma and decerebrate posturing is a grade 5 and portends a poorer outcome.

Missed or delayed diagnosis of SAH usually results from 3 errors:

1) failure to appreciate the spectrum of the clinical presentation,

2) failure to obtain a head CT scan or understand its limitations in diagnosing SAH, and

3) failure to perform a lumbar puncture or correctly interpret the results.

The most important source of missed diagnosis results from misconception that patients should  appear to be sick or have neurological findings, with altered mental status, when in fact about 40% of patients are awake, alert and neurologically intact.

For practice perspective, the vast majority of patients will be correctly diagnosed if all patients with thunderclap headache undergo a head CT, and lumbar puncture if the CT is done after 6 hours from the headache onset.

Diagnostic evaluation of SAH generally requires a noncontrast head CT and a lumbar puncture if the head CT is negative.  If both tests are negative, can  effectively eliminate diagnosis of SAH as long as both tests performed within 2 weeks of the event.

Written by Dr. Emmanuel Tanglao, MD

ERx Clinical Partners Medical Director

This is for informational purposes only. For medical advice or diagnosis, consult a physician