Clinical Case:
A 75-year-old-female who had been on hemodialysis for chronic kidney
disease for over four years visited her family physician’s clinic
complaining of fever. She denied any personal history of drug allergy or
anaphylaxis and no allergic reactions had previously occurred. She had a
history of hypertension and arteriosclerosis obliterans treated with
axillary-femoral bypass, for which she was prescribed aspirin 100mg per
day.
Empirically, she was given intravenous antibiotics (1g
cefoperazone-sulbactam) for a suspected bacterial infection three hours
after initiation of hemodialysis. A few minutes later, she proceeded to
develop periorbital edema, dyspnea, and altered consciousness, and her
blood pressure fell to 54/30 mmHg. Her family physician diagnosed her
with anaphylactic shock caused by the antibiotic and intramuscularly
administered 0.3 mg of adrenaline (1:1000 dilution) twice every five
minutes, as well as 5 mg of chlorpheniramine maleic acid, 20 mg of
famotidine, and 125 mg of methylprednisolone. A few minutes after
receiving adrenaline, the patient developed tachycardia with a pulse
rate of 140 beats/min and hypertension with a blood pressure of 208/88
mmHg. Thirty minutes after onset upon arrival of emergency medical
services personnel at the scene, her blood pressure fell to 94/44 mmHg.
She was admitted to our institution for further treatment one hour after
the incident.
En route to the emergency department, she appeared pale. She had a
Glasgow Coma Scale (GCS) score of 12 (E2V4M6), respiratory rate of 20
breaths/min, arterial oxygen saturation of 100% with oxygen delivered
through a face mask (3 L/min), pulse rate of 110 beats/min, blood
pressure of 104/78 mmHg, and body temperature of 37.1°C. Findings from
her physical neurological exam were unremarkable.
Laboratory test results demonstrated chronic kidney disease as indicated
by urea nitrogen levels of 17 mg/dL, elevated creatinine levels of 4.86
mg/dL, thrombocytopenia (blood platelets cell count of
9.0 × 104 cells/L), normal prolonged prothrombin time,
and activated partial thromboplastin time. Blood culture test did not
identify any bacteria. A computed tomography (CT) scan was conducted to
screen for causes of altered consciousness and acute shock other than
anaphylaxis. The CT scan revealed a hemorrhagic lesion measuring 9x9x5
mm in the right basal ganglia (Figure 1-A). We conducted conservative
treatment using nicardipine hydrochloride to promptly stabilize her
systolic blood pressure to under 140 mmHg, as well as tranexamic acid.
Neurological examination showed the patient failed to achieve complete
clarity of consciousness; she had a GCS score of 11 (E2V3M6) and her
left upper and lower limbs were paralyzed without sensory neuropathy
four hours after onset. We performed a follow-up head CT scan, which
showed that the intracerebral hemorrhage had increased in size to
52x35x30 mm (Figure 1-B). During the first few days, the patient
presented no additional neurological deterioration without further
expansion of the intracerebral hemorrhage.
The patient was transferred to the local rehabilitation hospital 28 days
after admission with weakness of the left upper and lower limbs, which
affected her daily life, and a modified Rankin Scale score of 5.