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Khalafalla Ahmed, Alrais, Beniamein, and Ahmad: Multiorgan dysfunction in Plasmodium vivax malaria complicated by a ruptured spleen


Non-falciparum malaria refers to a malarial infection caused by the Plasmodium species other than Plasmodium falciparum; this includes Plasmodium vivax, Plasmodium ovale and Plasmodium malariae.1,2 P. falciparum carries the highest risk of a fatal outcome. Patients infected by this species may deteriorate rapidly into a complicated and life-threatening condition. Of the non-falciparum malarial parasites, P. vivax may also cause severe and life-threatening illnesses.3

The number of people infected with P. vivax worldwide is estimated to be between 130 and 390 million, with 2.6 billion individuals living at risk of infection.4,5 Travellers visiting friends and relatives who live in endemic areas are particularly at risk of acquiring P. vivax.6

Patients who develop malaria become very sick, with flu-like symptoms including high-grade fevers and chills. Severe complications such as splenic rupture, acute respiratory distress syndrome (ARDS) and severe liver dysfunction are rare but not unknown.7,8 Although malaria can be fatal, early diagnosis and appropriate treatment are associated with a favourable prognosis.

Case report

A 29-year-old Pakistani male, a professional driver with no medical history of malaria, presented to Rashid Hospital, United Arab Emirates, having suffered epigastric pain, vomiting and diarrhoea for 1 day. He had also been experiencing intermittent fever, generalized body aches and weakness for 1 week. On initial examination he was lethargic and drowsy. He was hypotensive and tachycardic, with an initial blood pressure of 76/50 mmHg and heart rate of 95 beats per minute. His core body temperature was initially 36.4 °C, and then fell to 34.6 °C over the next couple of hours. The patient was resuscitated with 3 l of intravenous (i.v.) crystalloid fluids and his haemodynamic status improved after fluid boluses. All routine investigations, such as complete blood count, coagulation profile, liver function tests and renal function tests, were carried out on admission. A blood sample was sent for a peripheral smear for malarial parasites, which revealed P. vivax rings and gametocytes (Table 1).


Result of peripheral blood film for malarial parasites

Result date and time Description
9 November 2015, 08:45 Malaria preparation: malarial parasite not seen
29 October 2015, 10:26 Malaria preparation: malarial parasite not seen
28 October 2015, 08:17 Malaria pre preparation: positive
After reviewing the smear, scanty Plasmodium gametocytes seen
Corrected on 28 October 2015, 08:16: previously reported as malarial parasite not seen
26 October 2015, 05:08 Malaria preparation: positive
26 October 2015, 05:08 P. vivax: P. vivax – gametocytes
24 October 2015, 10:22 Malaria preparation: positive
24 October 2015, 10:22 P. vivax: P. vivax – ring form; P. vivax – gametocytes
23 October 2015, 02:30 Malaria preparation: positive
23 October 2015, 02:30 P. vivax: P. vivax – ring form; P. vivax – gametocytes

The patient was admitted to the high-dependency unit on 22 October 2015. On the second day after admission, he developed left upper-quadrant and epigastric pain as well as abdominal guarding and rigidity, and became hypotensive. Prompt investigation revealed that his haemoglobin (Hb) levels had dropped from 13.7 g/dl to 6.9 g/dl. Computerized tomography (CT) of the abdomen showed signs of haemoperitoneum, splenomegaly with an irregular outline and perisplenic haematoma highly suggestive of a ruptured spleen (Figure 1). Radiography of the abdomen was also performed, which revealed a mass in his left hypochondrium, probably due to splenomegaly (Figure 2).


Abdominal CT revealing haemoperitoneum and perisplenic fluid collection (splenic rupture).


Radiograph showing a mass in the left hypochondrium as a result of splenomegaly.


Following acute deterioration of the patient’s condition, he was transferred to the intensive care unit (ICU) on 24 October 2015. Urgent exploratory laparotomy was performed on the same day, and splenectomy was performed to secure haemostasis. After exploratory laparotomy and splenectomy, the patient was kept intubated and mechanically ventilated because of the development of an unstable haemodynamic status and ARDS (Figure 3).


Chest radiograph showing bilateral infiltration and fluffy shadows (revealing ARDS).


The patient required continuous renal replacement therapy (CRRT) until his renal function recovered approximately 1 week after admission to ICU. His liver function was significantly deranged, but improved during his hospital stay. His procalcitonin level was raised but normalized after a course of appropriate antibiotics (Table 2).


Other laboratory investigations

Investigation Date of test
22 October 2015 24 October 2015 25 October 2015 31 October 2015 5 November 2015 10 November 2015 16 November 2015 21 November 2015
HB (g/dl) 13.7 7.8 6.9 9 8.3 9.2 11.7 11.9
Haematocrit (%) 43 25 21.9 27.6 26.4 29.4 36 37
Platelets (1000/μl) 16 24 69 122 657 533 476 477
White blood cell count (1000/μl) 9.8 6.8 14.6 23.5 22.1 12.5 10.2 11.4
Blood urea (mg/dl) 46 87 73 49 238 115 76 55
Serum creatinine (g/dl) 2.7 3.5 4.3 1.4 (on CRRT) 5.4 3.3 1.8 1.6
Alanine transaminase (units/l) 35 3173 2010 125 156 52 94 101
Aspartate transaminase (units/l) 42 2092 1223 231 64 64
Bilirubin (total) (mg/dl) 4.9 5.1 4.8 15.3 12.3 5.4 3 2.6
Procalcitonin (ng/ml) 36 57.97 65.14 6.09 3.63 0.83 0.22
Serum sodium (mmol/l) 138 138 139 133 132 133 135 136
Serum potassium (mmol/l) 4.7 4.1 3.8 4.4 3.8 4.3 4.9 4.5

He was started on antimalarial treatment with 600 mg of i.v. quinine dihydrochloride every 8 hours for 1 week and appropriate antibiotics: 600 mg of i.v. clindamycin every 8 hours and 2.25 g of i.v. piperacillin and tazobactam every 8 hours for 1 week for concurrent sepsis initially on admission to the ward. Later, 15 mg of oral primaquine was given every 12 hours for 2 weeks.

Lung function and renal parameters improved gradually over a period of around 2 weeks under the care of the ICU. The patient was transferred to the medical ward after 16 days in ICU and discharged home after 28 days in hospital, without any further complications.


Plasmodium vivax and P. ovale infections are generally benign, and complications leading to significant morbidity and mortality are relatively uncommon.9 Although P. vivax malaria is considered to be benign, it has been increasingly reported to cause various manifestations of severe disease, including thrombocytopenia, cerebral malaria, acute renal failure, hepatic dysfunction and pulmonary manifestations, such as ARDS, leading to a poor prognosis.7,8 The underlying mechanisms of severe manifestations are not well understood. Prompt and effective treatment of these cases can prevent a poor outcome.

A review of the literature identified only 22 cases of malaria resulting in spontaneous ruptured spleen since 1960. P. falciparum was the predominant organism involved, followed by P. vivax and P. ovale. This may be a result of under-reporting, as malaria is the most common cause of a spontaneous ruptured spleen.10

The exact mechanism of ruptured spleen in malaria is not known but three explanations have been put forward: (1) an increase in intrasplenic tension as a result of cellular hyperplasia and engorgement; (2) compression of spleen by the abdominal musculature during physiological activities such as sneezing, coughing, defecation, etc.; and (3) vascular occlusion due to reticuloendothelial hyperplasia, resulting in thrombosis and infarction. This leads to interstitial and subcapsular haemorrhage and stripping of the capsule, which leads to further subcapsular haemorrhage. The distended capsule finally gives way and ruptures.9

In our patient, Hb fell to 6.9 g/dl due to acute haemorrhage caused by splenic rupture, as confirmed on exploratory laparotomy, which was corrected with transfusions of packed red cells. The patient had also severe thrombocytopenia on admission, probably due to hypersplenism, and acute haemorrhage secondary to his ruptured spleen.

Acute respiratory distress syndrome is a severe form of lung injury that can occur in patients with malaria. The pathogenesis of ARDS in malaria is multifactorial; precipitating conditions include sequestration of parasite-containing erythrocytes, host immunological reaction, coexistent sepsis and pulmonary infections that ultimately cause increased alveolar permeability induced by cytokines. ARDS is also known to occur in P. vivax infection, but only rarely, and shows much less microvascular sequestration than P. falciparum malaria. Sequestration of parasites in the lungs accompanied by the post-treatment inflammatory response is the likely explanation of lung injury in P. vivax malaria. Patients with ARDS complicating vivax malaria have a better prognosis than those with ARDS as a result of falciparum malaria.7,8,11,12

Renal function was deranged in our patient as a result of acute kidney injury caused by shock due to acute haemorrhage following rupture of the spleen. The patient required CRRT until his renal function recovered, approximately 1 week after admission to the ICU. The patient’s liver function was also significantly deranged by shock of the liver as a result of acute haemorrhage due to his ruptured spleen. The patient’s procalcitonin level was raised initially but normalized after a course of appropriate antibiotics.

In summary, our patient developed complications of malaria, including a ruptured spleen, ARDS, severe liver dysfunction and renal impairment, which are rare but have been previously well reported in the literature.


Severe malarial infection with P. falciparum is associated with severe illness and a poor prognosis. P. vivax malaria is a benign condition, but is also associated with severe complications such as a ruptured spleen, ARDS, acute kidney injury and severe liver dysfunction.

Although detection of P. vivax parasites in a blood smear is the standard method of diagnosis justifying the initiation of antimalarial drug therapy, repeated polymerase chain reaction testing is required to exclude the possibility of coinfection with P. falciparum and to confirm that all complications are attributable to P. vivax.



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