<Case Presentation
>
This
65-year-old man was admitted on October 9th, 2001 because of
general malaise and jaundice for half a month, and fever for
about 3 days.
He had worked in Nigeria since
this February until he returned to Taiwan on September 26th.
He was found yellowish looking by his family about half a
month ago. He began to experience general malaise and poor
appetite gradually. Dark-color urine was also noted. Fever and
chills occurred on October 4th. On the following days, he felt
nausea, vomiting, and diarrhea about 4 times a day. He went to
a local clinic and intravenous fluid was given under the
impression of common cold. He visited our Emergency Department
on October 9thdue to persistent fever.
He had neither diabetes mellitus,
hypertension, nor previous history of hepatitis. He denied the
use of alcohol, drugs, or smoking.
At the Emergency Department, his
body temperature was 38.1℃, blood pressure was 155/87mmHg,
pulse rate was 133/min, and respiratory rate was 24/min. His
consciousness was clear. The conjunctiva was pale and sclera
icteric. The neck was supple. The breath sounds were clear.
The heart beats were regular; no murmurs were heard. His liver
was palpable; the liver span was 11 centimeters at the right
middle clavicular line. The spleen was palpable. There was
right upper quadrant tenderness but no rebound tenderness.
Cyanosis, edema, skin rash, petechiae, and ecchymosis were not
seen.
The liver function test revealed
a total bilirubin of 5.19 mg/dL, a direct bilirubin of
2.0 mg/dL, and mildly elevated AST of 52 IU/L and ALT of 38
IU/L. His renal function was BUN of 34.2 mg/dL and Cre 0.76
mg/dL. The leukocyte count was 5230 /uL (band 37%, segment
43%, monocyte 4%, lymphocyte 13%, and atypical lymphocyte 2%).
The hemoglobin was 13.9 g/dL and hematocrit 38.6%.
Marked thrombocytopenia was found with a platelet count of
9000/uL. Urinalysis showed that protein was > 300 mg/dL,
occult blood, 1+ bilirubin 3+, urobilinogen 1.0 EU/dL, and RBC 0-1
per high power field. His chest radiography on admission was
normal.
Infection of Plasmodium
falciparum was determined after we obtained a thick blood
smear, which disclosed intraerythrocytic malaria parasites
with predominantly blue ring forms. The initial treatment
included hydration and oral mefloquine (750 mg as a single
dose, followed by 500 mg in 6 hours and 250 mg in 12 hours)
due to high resistant rate of malaria to chloroquine in
Nigeria. He still had fever over the next two days of
admission, and anemia due to hemolysis developed
progressively. He had received transfusion therapy with packed
RBC and platelet for the anemia and thrombocytopenia. On the
third day of admission, the blood smear revealed decreased
parasite load (less than 5% of erythrocytes were infected).
However, the patient suffered from altered mentation, seizure,
lactic acidosis and impaired renal function (BUN 71.0 mg/dL
and Cre 1.88 mg/dL). The cerebrospinal fluid examination
showed that leukocyte count was 2 lymphocyte per high power
field, protein was 76.9 mg/dL, and sugar was 81 mg/dL. The
magnetic resonance imaging of brain had not disclosed any
abnormality. Under the impression of cerebral malaria, he was
transferred to intensive care unit, and received intravenous
quinidine sulfate 10mg/kg every 8 hours and doxycycline 100 mg
every 12 hours. The consciousness recovered on the next day,
and renal function improved gradually later. Because the
patient had recovered consciousness and could take oral
medications, the medications were switched to oral quinine
(600 mg tid) and doxycycline (100 mg bid).
The next day after medication switched to oral
quinine and doxycycline, sudden onset of generalized tonic-clonic
seizures occurred, accompanied with recurrent fever,
shock status, and respiratory distress with desaturation.
The patient underwent intubation with ventilator support
and received vasopressor for hemodynamic maintenance.
The chest radiograph revealed diffuse pulmonary infiltrates
over bilateral lung fields. The measurements of pulmonary
artery catheter favored distributive shock and non-cardiogenic
lung edema (pulmonary artery wedge pressure 11 mm
Hg, cardiac index 6.36 l/min/m2, and systemic vascular resistance
index 704 dyne/sec/cm2/m2). Anemia, thrombocytopenia,
and hyperbilirubinemia persisted during this period.
Although the blood smear still revealed decreased parasite
load (less than 1% of erythrocytes were infected), we switched
anti-malaria therapy to intravenous artesunate. An
antibiotic with ceftazidime was also used because nosocomial
pneumonia could not be ruled out. His condition was stabilized
gradually over the next week. The hemodynamics and oxygenation
improved, fever subsided, and hemogram recovered. The blood
smear showed no more malaria parasites after 5-day use of
artesunate. The chest radiograph became clear. He eventually
underwent successful extubation on Oct 18th. Liver and renal
functions gradually improved and fever subsided. He was
transferred to a general ward on Oct 19th and was discharged
on Oct 24th.
病案分析
本病例是一境外移入之惡性瘧原蟲(Plasmodium
falciparum)感染,併發抽搐(convulsions)、休克(shock),以及非心因性肺水腫(noncardiogenic
lung
edema)。病患一開始的症狀是疲倦、胃口變差、發燒、噁心、嘔吐以及腹瀉。因為這些症狀是nonspecific,常常會被誤認為是感冒或者是腸胃炎。
現今是地球村的時代,國人因為多種因素會前往各種疫情的地區,所以醫師應更警覺地追溯病人的travel
history。現病史中問到病人剛從奈及利亞回來沒多久,再加上有明顯的發燒及黃疸,此時診斷就呼之欲出。血液抹片的檢查可以確定出是哪一種瘧原蟲的感染。
瘧疾在熱帶地區仍造成相當多人感染及死亡。台灣的瘧疾病患絕大多數是境外移入(imported)。
在過去二十年來,惡性瘧原蟲對chloroquine的抗藥性,已成為一個全球廣泛注意的問題,前往瘧疾疫情地區(endemic
areas),應事先開始預防性的服用抗瘧疾的藥物以防止感染。
惡性瘧是瘧疾感染中症狀最嚴重的一種,然而經過即時的診斷及適當的治療,在沒有併發症下,死亡率約千分之一。但是一旦發生嚴重的併發症(如本例病人),沒有完善的治療,死亡率相當高。受惡性瘧原蟲感染的紅血球會附著於血管壁的內皮細胞,而且紅血球也會相互黏著形成如花束般的一團,如此可能堵住血液循環而造成許多病症。本例病患先發生抽搐經診斷是腦性瘧疾(cerebral
malaria),在病患清醒後於治療過程中,再次發生抽搐並進而發生休克以及非心因性肺水腫。其真正的原因並不清楚,但研究顯示大量釋放出的細胞激素(cytokines)及發炎介子(inflammatory
mediators)可能是造成此併發症的原因。
本病例為少見的惡性瘧併發症。在病患發生抽搐後即早住進加護病房小心監測及治療,在發生休克及非心因性肺積水,給予PEEP以及在Swan-Ganz
Catheter監測下小心給予輸液治療,而能成功治療病人。
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