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A 68-year-old man presented to the
emergency department of a teaching hospital in Taipei because
of high fever, tachycardia, consciousness disturbance, and
generalized muscle rigidity. According to his caregiver's
statement, he was found lying on the bed groaning, with
shivering, tachypnea, and unresponsive before he was sent to
the hospital.
He had a depressive disorder and
had been followed regularly at a local psychiatric center for
six years. Besides, he had chronic hepatitis B and had been
diagnosed as pneumoconiosis. Ten days before this admission,
he was brought to the psychiatric clinic of our hospital
because of a deterioration of his depressed mood. Venlafaxine
(Efexor XR), amantadine (PK-Merz), clonazepam (Rivotril) and
zopiclone (Imovane) were administered and he had good
compliance to these drugs. He received influenza vaccination 8
hours prior to his emergency visit.
PHYSICAL EXAMINATION
Temperature was 39.7 °C, blood pressure was 162/92 mm Hg,
pulse was 142 beats/min, and respiration was 30 breaths/min.
The patient appeared acutely ill, with sweating and severe
shivering. The sclerae were not icteric. The pupils were
isocoric with prompt light reflex. The neck was stiff. The
neck veins were not engorged and no lymphadenopathy was noted.
The respirations were rapid and shallow The lungs were clear.
The heart had no murmur. The abdomen was soft and flat without
tenderness. There was no hepatosplenomegaly. Persistent tremor
and cogwheel rigidity of four extremities were noted, and the
lower extremities were more severely involved. There was no
pitting edema, bruises, skin rash or wounds.
LABORATORY FINDINGS
Laboratory findings were as
follows: white blood count, 6,270/μL with 90% neutrophils;
platelet count, 264,000/μL; hemoglobin, 12.5 g/dL; blood
glucose, 256 mg/dL; sodium, 141 mEq/L; potassium, 3.88 mEq/L;
total calcium 2.22 mM/L; asparate aminotransferase. 69 U/L;
total bilirubin 0.9 mg/ L; blood urea nitrogen, 23.5 mg/L;
creatinine, 1.3 mg/L; albumin, 4.0 g/dL; creatine kinase, 1122
IU/L with a MB fraction of 21.5 IU/L. Arterial blood gas
analysis when breathing 3 liters/min oxygen via a nasal prong
showed pH of 7.468, PaO2 126 mm Hg, PaCO2 22 mm Hg and HCO3-
16 mEq/L. The ammonia
level was within normal limit and
the c-reactive protein was not
elevated.
The
urinalysis was positive for occult blood but there was no
hematuria, pyuria or ketonuria. The chest radiograph (Figure 1)
showed bilateral reticulonodular infiltrates compatible with
his previous diagnosis of pneumoconiosis. Computer tomograogy
(CT) of the brain (Figure 2
) was negative. A lumbar puncture yielded
clear, colorless cerebrospinal fluid (CSF) that contained only
one lymphocyte per cubic millimeter. The open pressure was
within normal limit. The glucose and total protein levels of
the CSF were 92 mg/dL and 67.4 mg/dL, respectively.
Question: What is the most likely diagnosis of
this patient ?
HOSPITAL
COURSE
The patient
was admitted to our intensive care unit because of drowsy
consciousness and clinical pictures mimicking SIRS (systemic
inflammatory response syndrome). Intravenous ceftriaxone and
penicillin-G were administered initially but was discontinued
soon after infection was excluded. The rhabdomyolysis was
managed with vigorous hydration and urine alkalization, as
well as cautious monitoring of serum potassium and phosphate.
However, his hyperthermia persisted despite acetaminophen,
NSAID and ice pillow use.
A detailed review of his chart at
the psychistric clinic revealed the dosage of venlafaxine was
increased from once to twice daily and amantadine from half a
tab thrice daily to one tab twice daily three days before
hospitalization. After consultation with his psychiatrist, we
discontinued venlafaxine but kept the use of amantadine.
Bromocriptine was administered orally. Besides,intravenous
lorazepam (Ativan) was given intermittently for the control of
his tremor and rigidity.
Sixteen hours after admission, the
body temperature and the heart rate (respirations?) began to
fall. In addition, his muscle rigidity improved gradually. One
day later, the vital signs were almost normalized. The serum
creatine kinase reached a peak level of 25,934 IU/L at the
24th hour, but the renal function remained normal. His
consciousness improved as well and was able to answer simple
questions on the third day. Bromocriptine was discontinued and
he was transferred to the general ward on the third hospital
day. He was discharged on the 7th
hospital day without
any neurological sequel or organ
dysfunction.
| DIAGNOSIS: |
Neuroleptic malignant
syndrome (NMS), |
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possibly
venlafaxine-related |
 案例分析
此案例敘述一個68歲的病患來急診時有高燒，心跳過速及全身僵硬，合併橫紋肌溶解的症狀。過去的病史顯示此為一罹患憂鬱症案例，長期服用Venlafaxine,
Auantedine,
Clonazepame及Zopiclone。NMS主要表徵為全身僵硬，意識不清，及高燒不退。發生率為0.2%，在任何年齡都有可能發生。診斷的依據，病人的用藥史，及潛在的疾病最重要。除了與多巴胺受體(Dopamine-2
receptor)抑制劑有關外，一些止吐藥如metoclpramide,
prochlorperqzine及鎮靜、麻醉劑如droperidol,
promethazine也容易誘發NMS，通常在用藥後30日內發病。一般認為正常劑量也會引發NMS，尤其在較高劑量，調藥速度過快，或靜脈注射時較易發生。其合併症則為廣泛性的腦傷害和肌肉壞死，如未經適當的治療可能致命。治療的原則，首先必須有想到此症的可能性，停掉可疑的藥物，然後可加bromocriptine,
amantadine或其它Depamine
agonists如症狀嚴重，可用Dantrolene
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Case Discussion
繼續教育考題