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E M E R G E N C Y M E
D I C I N E
HISTORY:
58 y.o. black M is BIBA with c/o disorientation and L sided weakness and
a L eye gaze. He was living @ Barrier Free Living (a home for independent
people who require a structured home life) when friends noted the sudden
onset of mental status change and confusion. EMS was alerted; BLS found
the patient to have HA on the scene with a BP 220/110 110P 20R GCS=15.
EMS reports that as the patient was being brought in, he appeared to have
had a clonic-tonic seizure; the episode lasted a few seconds and he stopped
seizing on his own.
Currently, the patient is talking and has complaints of severe headache
and is disorientated to time, but is conscious of place and name. Otherwise,
the patient is unable to furnish any medical history, other than high
blood pressure and that he was recently taken off of one of his HTN meds-
cardizem.
Meds- cardizem & propranolol.
Allergy- NKDA
PMHx- HTN
PSHx- none
SoHx- No smoke, ETOH, drugs. Travel- none. Pets- none.
PHYSICAL:
240/120: BP equal in both arms 114P 18R T98.9
PulseO2-100% (non-rebreather). FS-120
WD/WN Black M lethargic
HEENT- NC/AT. Eyes are deviated to the left, but reactive to light and
equal. Not cooperative with fundus exam.
Chest- CTA No W/C/R
Cor- RRR nl S1S2 No M/G/R
Abd- Soft, nontender, +BS, no masses
Rectal- guaiac neg, good tone.
Ext- 2+ pulses x 4 ext.
Neuro- A&O x 2. Lethargic. Spontaneously moving all extremities; sensory-
non-cooperative. Reflexes- non-cooperative.
At this point, pt was started on a nitroprusside drip, given benzodiazepines
for sedation and seizure prophylaxis, and intubated for control of airway
in preparation for CT-scan of the head.
Dilantin bolus given for seizure control.
ANCILLARY TESTS:
EKG- marked LVH. NO ÆST, or dec. T wave.
CXR- post-intubation, good tube placement, no I/E
LABS-
ABG- 7.50/38/526/29.6 (HCO3)/BE 6.6/99.9%
CBC: WBC-6.7 HGB-15 HCT-43 PLT-175 G48 L39 M9.4
SMA-7: NA-139 K-3.1 CL-94 HCO3-33 BUN-15 CRE-1.3 GLC-129
PT/PTT/INR 11.8/29.5/1.0
UA- wnl.
CT-head- revealed an old L parietal lobe infarct, but no new masses or
shifts.
MICU called and admitted for continued care.
HOSPITAL COURSE:
Pt was seizure free in MICU and dilantin serum levels were therapeutic;
pt was transferred to neurology service the next day. His neurologic findings
resolved with no apparent residual deficits.
LABS-
Na-139, K-2.7, Cl-98, HCO3-30, BUN-14, Cre-1.3, Glc-145
Ca-8.6, PO4-4.1, Mg-1.6, UricAcid-3.9, TP-6.8, Alb-3.5,
Glob-3.3, LDH-265, AST-36, ALT-22, ALP-78,
Tbili/direct-0.4/0.2, Chol-148,
CK-316, MB-3.9, CI-NK
Aldosterone-25 (nl supine < 8),
Renin-0.2 (nl supine < 2),
ACE-wnl,
cortisol-wnl.
24-Urine- All wnl.
Ucre-1.4,
Umeta-86,
Umeta tot-281,
Unormeta-195,
UVMA-2.4

Adrenal vein sampling performed to rule out
adrenal hyperplasia vs adenoma
Normal levels of aldosterone is less than 20 ugm/ml. Clearly, levels of
both adrenals were elevated; and therefore, bilateral adrenal hyperplasia
was diagnosed. Further management problems encountered were the titration
of 6 antihypertensive medications to lower the patient's BP to 190/100.
The patient was discharged on dilantin, monopril, atenolol, lasix, clonidine
patch, cardizem, DSMO. At home, the patient washed off the clonidine patch
by mistake; however, he did not realize that he had washed off the medications.
The patient returned to the emergency room via EMS with cardiac chest
pain, changes in his EKG, and a BP of 240/120. At this second presentation,
the patient had elevated CPK-MB and cardiac enzyme index was elevated.
A cardiac catheterization showed clean coronaries and a presumed rebound
hypertensive crisis was given for his second admission. The patient was
titrated on clonidine and discharged home with close Nephrology follow
up. To date, the patient is doing well with control over his hypertension.
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