Severe Thrombocytopenia in a Child With Typhoid Fever: A Case Report

Mohammed Al Reesi; Glenn Stephens; Brendan McMullan


J Med Case Reports. 2016;10(333) 

In This Article

Case Presentation

A 4-year-old Asian boy presented to the emergency department at a tertiary children's hospital in Sydney, Australia, 1 day after returning from travel to Bangladesh with a persistent fever for 10 days. He had visited Bangladesh with his parents and stayed for 8 weeks. He had vomiting, diarrhea, and fever 3 weeks after arriving in Bangladesh, for which he was given oral ciprofloxacin for 3 days. The vomiting and diarrhea resolved after 1 week, but he continued to have intermittent fevers up to 38 °C (100.4 °F) for an additional 2 weeks. During the last 10 days of his stay in Bangladesh, his fever became persistent, with peaks of 40 °C (104 °F). He had reduced oral intake and constipation, but no vomiting. His mother reported that she had developed self-limited vomiting and diarrhea for a few days after the onset of his symptoms. The family denied eating street food or drinking tap water in Bangladesh. There was no history of contact with patients with tuberculosis. The child had been born in Australia to Bangladeshi parents, and his immunizations were up to date, according to the Australian schedule. He did not receive any travel vaccines prior to travel or malaria prophylaxis. His medical history was unremarkable apart from mild asthma.

In the emergency department he appeared unwell and moderately dehydrated. He was febrile at 39.8 °C (103.6 °F), tachycardic with a heart rate of 160 beats per minute, and his respiratory rate was 32 breaths per minute. There was no icterus, pallor, or lymphadenopathy. A skin examination did not reveal any rash, petechiae, or bruising. A chest and cardiovascular examination revealed no abnormalities. His abdomen was soft, mildly tender, and distended with no organomegaly. There was no clinical ascites and his bowel sounds were present. He was alert and oriented, with a normal neurological examination. He had no bone or joint pains or swelling. Initial investigations showed anemia, leukopenia, and thrombocytopenia. His hemoglobin concentration was 102 g/L and reached a nadir of 89 g/L on day 11 of admission. He had a nadir white cell count of 4.30 × 109/L (neutrophils 2.6 × 109/L and lymphocytes 0.9 × 109/L) on presentation, which gradually improved to 11 × 109/L by day 11. His initial platelet count was 97 × 109/L. His renal function was normal apart from mild hyponatremia, while his liver function tests showed hypoalbuminemia and mild transaminitis with normal bilirubin concentrations. His C-reactive protein level was elevated at 92 mg/L. Considering his clinical presentation, travel history, and the initial investigation results, the differential diagnoses included typhoid fever, malaria, and dengue fever. We ordered a blood culture, and thick and thin blood films for malaria parasites and dengue IgM, IgG, and NS1 antigen. He was then commenced on ceftriaxone intravenously and admitted to our hospital. There were no malaria parasites seen in two films and dengue serology was also negative. The following day his stool and blood cultures grew Salmonella Typhi. The organism was reported to be susceptible to ceftriaxone and azithromycin, with decreased susceptibility to ciprofloxacin. It was reported to be resistant to ampicillin, chloramphenicol, and trimethoprim.

Our patient continued to have fever spikes to 39–40 °C every 4 hours after admission until the fifth day, when the frequency of fever decreased to three spikes daily. Further improvement was noticed by day 9, with temperature spikes decreasing to twice daily and less than 39 °C. He required intravenous fluids for a short period to correct his dehydration until his oral intake gradually normalized over the first week in hospital. In addition, he received an albumin infusion on day 5 after he developed clinical ascites with a further drop in his albumin to 17 g/L. Thrombocytopenia was notable in our patient. His platelet count initially fell steadily and reached a nadir of 16 × 109/L on day 5 despite appropriate antibiotic therapy (Fig. 1). He was monitored closely for complications associated with thrombocytopenia: his sensorium remained intact and he did not develop petechiae, bruising, or rectal bleeding during admission. There was no sign of intestinal perforation, with normal bowel sounds and an absence of bloody stool. At this stage, we considered whether additional therapy for thrombocytopenia would be required, such as platelet transfusion. Upon discussion with our infectious diseases team, it was decided to treat him conservatively with close observation and not to give him a transfusion. His platelet count was monitored on a daily basis, began to improve on day 6 of admission, and finally normalized on day 11 and then climbed to supra-normal levels by day 15. Likewise, his transaminases were abnormal throughout admission, peaking on day 5 (Fig. 1), but started to improve before discharge. By day 9 of admission, his oral intake improved and oral azithromycin was added to transition to oral therapy. He completed a 12-day course of ceftriaxone in hospital and was discharged in a good condition, although he still had occasional fever spikes to 39 °C. He continued to have intermittent elevated temperatures (<38 °C) at home, but his parents reported that he returned to his previous energy level and activity. After he completed a total 7-day course of azithromycin, he was reviewed in an outpatient clinic where he was afebrile with a normal examination.

Figure 1.

Progress of thrombocytopenia and transaminitis over time