FALCIPARUM MALARIA PRESENTING AS ACUTE PANCREATITIS

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Barik B.K, Dhar S.K.

ABSTRACT:

            We report a case of Acute pancreatitis in a case of falciparum malaria. The incidence of other complications are common. The mechanism of this rare complication and its pathophysiology is reviewed. ( The Ind. Pract. 2005; 58(10): 649-651).

KEYWARDS:

            Malaria (Plasmodium Falciparum Malaria), Complications, Acute Pancreatitis, Serum Amylase, Serum Lipase.

INTRODUCTION:

            Malaria, a burning problem in tropical countries and a disease of global concern has a major preponderance in India affecting life of all ages and races. It complications are responsible for taking away a  major fraction of patient death in our country. The acute and chronic complications are many. As far as falciparum malaria is concerned it has diverse life threatening complications. Acute pancreatitis is very rare but devastating complication of falciparum malaria which we have put as a case report.

 CASE REPORT:

A 41 year old male presented in general medicine ward in October 2004 with history of fever of 5 days which was associated with chill and rigor. There was yellow coloration of urine and conjunctiva for 3 days and gradual decrease of urination for 2 days. There was 5-6 episodes of loose motions and vomiting and pain abdomen (confined to epigastic region) for 10 hours before admission. The patient was not an alcoholic. There was no previous such history of pain abdomen. There was no history of trauma to abdomen. He is not a known case of DM, HTN, SCD APD. There was no history of taking any drug.

On examination the patient was average built, conscious with moderate pallor moderate icterus with mild oedema (bilateral pedal) no lymphadenopathy with a pulse rare 92 per minutes, regular, BP 100/70 mm of HG, without any signs of dehydration. Abdominal examination revealed mild distension and diffuse tenderness maximum at epigastric area, smooth tender hepatomegaly ( 5 cm below the costal line) moderate non tender spenomegaly (3 cm below the left costal margin), mild ascites and diminished bowel sound. Cardiovascular system, respiratory system and other systemic examination revealed no abnormality.

INVESTIGATION

HB- 9.8gm%

TLC – 10,200/mm²

DC – N69%, E-1%, L30%, B0%, M0%

Widal test – Negative

Microfilaria – Negative

Serum Bilirubin – Total 13.3mg%, Direct 10.4%

RBS – 172mg%

SGOT – 11IU/L

SGPT – 138IU/L

Serum Alkaline Phosphatase – 110 IU/L

S. Urea – 106mg%

S.Creatinine – 4.2mg%

Serum Amylase – 2050 IU/L

Serum Lipase – 3050IU/L

Serum Ca++ - 7.2gm%

HBs Ag – Negative

HCV Ag – Negative

Malaria Parasite – Slide +ve

QBC – pfr (++)

ICT – pfr (+)

Ultrasonogram revealed hepatosplenomegaly and features of acute pancreatitis and mild ascites. CT scan of abdomen also revealed hepatosplenomegaly ascites and acute pancreatitis. 

On the basis of blood report patient was treated along the line of complicated malaria with artesunate, injection cefipime, metronidazole injection, inject able pantoprazole, intravenous fluid and one unit of blood transfusion. The patient was conservatively managed for acute pancreatitis and nasogastric tube aspiration and nil orally for 5 days. The patient recovered within a span of 7 days after which the MP was negative. Serum amylase, serum lipase, Urea, Creatinine and bilirubin came down to 100IU/L, 230 IU/L, 28mg %, 0.8 mg%, 4.2 mg% respectively on 7^th day. Repeat USG of abdomen revealed only mild hepatomegaly. The patients was relieved on 14^th day of admission.

DISCUSSION:

            Pancreatitis clinically presents with upper abdominal pain accompanied by elevated levels of pancreatic enzymes i.e amylase and lipase. The type such as acute chronic haemorrhagic, necrotic are distinguished by history, clinical , biochemical and radiological findings.

            Acute pancreatitis presents as neusea, vomiting , anorexia, abdominal pain. Out of numerous causes of acute pancreatitis malaria is rare. But it must be looked for in tropical country like India with high prevalence of malaria.

            Falciparum malaria is the deadest among all other types of malaria with varied complications, multiorgan involvement and diverse sequlae. The parasite may affect pancrease causing acute pancreatitis or acute haemorrhagic pancreatitis. The clinical and laboratory findings follow similar pattern of other causes of acute pancreatitis.

The pathogenesis may be initiated by sequestration of parasite in the organ, blood vessels or ducts, damaging acinar cells by premature activation of digestive enzymes with cells. The damaged acinar cells initiate inflammation, activation of platelets and compliment system, which leads to release to cytokines (e.g TNF - a, IL – 1, NO, PAF), free radicals and other vasoactive substances. These further directly damage the gland and may cause pancreatic oedema, necrosis, ischaemia and capillary leak syndrome. Tehse lead to a vicious inflammatory cycle damaging further pancreatic tissue. Association of sepsis further leads to organ damage and complications.

Malaria presenting with classical symptoms and signs of acute pancratitis along with other organ involvement may be difficult to correlate. The abdominal pain may be sharp, sudden or constant may be localized to epigastric,periumbilical, block or lower chest. But common presentation in malaria is fever, icterus with distended abdomen, diffuse or localized tenderness. Grey Turners signs or Cullen sign may be noted in advanced cases.

Blood count and chemistry panel usually distinguishes pancreatitis from other acute abdominal causes, Test of malaria (MP, Slide , QBC, ICT) determines malaria aetiology, Increased TLC, Hyperglycaemia, decreased Ca++, Increased alkaline phsophatase, S. Amylase, S. Lipase reflects pancreatic damage.

Serum amylase has low sensitivity (75-92%)and Specificity (20-60%) but is used to confirm acute pancreatitis , when upper limit is raised 3-6 times of normal specificity increases. Serum amylase level is raised 2-12 hours after pancreatic insult and peaks 12-71 hours after. 

Serum lipase having sensitivity 86-100% and specificity of 50-99%. Serum lipase raised 4-8 hours after signs and symptoms and peaks at 24 hour and decrease over 8-14 days. 

Other recent markers are immunoreactive cationic trypsin, pancreatic elastase – 1 and phospholipase. 

Although USG and Ct scan of abdomen makes the diagnosis easy, cholangio-pancreatography may be accompolished bu ERCP or MRCP. 

The primary treatment of acute pancreatitis with malaria is to treat the cause i.,e malaria. The treatment of acute pancreatitis is primarily supportive providing adequate hydration, pain relief and pancreatic rest by nasogastric suction and nil orally. Antibiotics are added to prevent sepsis or necrotic pancreatitis with setting of multiorgan involvement.

The prognosis of acute pancreatitis with malaria depends on the stage of presentation, haemorrhagic pancreatitis bears poor prognosis.

CONCLUSION

            Falciparum malaria which has various complications may present as an acute pancreatitis, along with other organ affection. This is a rare condition and must be in mind of clinicians when patient presenting with clinical features of malaria, with pain abdomen , vomiting and localized abdominal tenderness.

            A high index of suspicion and thorough clinical examination and investigation are the ways to diagnose the complication i.e, acute pancreatitis. Specific antimalarial drugs are the primary modalities of treatment, along with the conservative management for acute pancreatitis.

REFERENCE:

1.      Von Sonnenberg F, Los Cher T, Nothdurgt HD, Prufer L @ Pubmed . PMID : 3519146.

2. Michelle M, Piet Zak MD (1) Dan W Thomas MD (2).