This paper reports a case of meningococcal septicaemia. This case shows that normal investigations may provide the unwary clinician with an unfounded reassurance when dealing with children with this serious infection.
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A general practitioner saw a 5 month old girl at morning surgery. She had been seen earlier in the week with diarrhoea and vomiting. This was thought to be attributable to viral gastroenteritis. The gastrointestinal symptoms had settled, but the child had now developed a fever and was becoming increasingly irritable. The child was reviewed again after two hours. She was not settling so the GP arranged admission to the paediatric acute admission unit at the local district general hospital.
On arrival the baby was alert. Her temperature was 38.4°C, respiratory rate was 64 breath/min, pulse was 170 beat/min. and her oxygen saturations were 96% on air. Her breathing was noisy because of nasal secretions. The chest was clear and heart sounds were normal. Her abdomen was soft and non-tender. Her mucus membranes were moist and the capillary refill was less than two seconds centrally. Two 3 mm diameter pale, blanching, erythematous macules were noted in her left flank.
A diagnosis of viral upper respiratory tract infection with a non-specific rash was made. Paracetamol was given to treat the fever and intravenous fluids were given to prevent dehydration.
Blood investigations showed Na+ 136 mmol/l, K+ 3.9 mmol/l, Ur 1.0 mmol/l, HCO3− 20 mmol/l. C reactive protein (CRP) was less than 10 mg/l. Unfortunately, the full blood count sample clotted during transit to the laboratory. A lumbar puncture was performed to exclude meningitis. Cerebrospinal fluid was clear and colourless. Microscopy and biochemistry of cerebrospinal fluid was normal.
Within the next hour the patient was reviewed by the on-call consultant who felt that this could be meningococcal septicaemia. Blood was taken for culture and polymerase chain reaction for meningococcus. Intravenous cefotaxime was given followed by a fluid bolus.
Over the next two hours she started to deteriorate rapidly. She responded to voice and non-blanching purpura developed on her torso, face, and neck. Capillary refill was now five seconds. Supplemental oxygen was given. A capillary sample was sent for blood gas analysis. This showed pH 6.91, pO2 7.64 KPa, pCO2 9.26 KPa, HCO3 13.5 mmol/l base excess −19.9 mmol/l on 10 litres of oxygen per minute. Blood was sent for clotting screen, which showed prothrombin time 19 s and activated partial thromboplastin time 105 s. A further fluid bolus and 4.2% sodium bicarbonate solution were given. Fresh frozen plasma was also given to correct the abnormal clotting.
The child was now beginning to tire. Her pulse was 194 beat/min, respiratory rate was 73, and blood pressure was 69/47. Dobutamine was started via a peripheral line and a rapid sequence induction was performed by the on-call consultant anaesthetist.
Two hours after starting ventilation the child had an episode of sinus bradycardia that was treated with intravenous atropine. She responded initially but 30 minutes later she had an asystolic arrest and never recovered. This 5 month old girl died within nine hours of admission.
Postmortem examination was declined. Blood cultures grew group B meningococcus confirming the diagnosis of meningococcal infection.
Despite treatment that was not far removed from current guidelines, a febrile but apparently well child, with a normal CRP and lumbar puncture, who was frequently reviewed by a paediatric senior house officer, consultant, and experienced paediatric nurse died from meningococcal septicaemia within nine hours of presentation.
In a tragic way this case demonstrates a number of learning points. The initial clinical features can be vague. Our catchment area contains about 300 febrile children every day. The task of identifying high risk patients is obviously difficult. We suggest that all children who have a feverish illness without a clear infective focus should be suspected of having meningococcal septicaemia. These initial diagnostic difficulties should teach us to become sympathetic for clinicians who get caught out.
At presentation the rash consisted of two blanching macules. This is not the characteristic rash that is associated with meningococcal septicaemia. However, in the early stages of disease a blanching maculopapular rash can occur in about 17% of patients.1 The confidence of the clinician should not be placed in this clinical sign alone.
In this case all initial investigations were normal. This can easily provide the unsuspecting clinician with ungrounded reassurance. Bonsu and Harper found that 64% of 170 patients with bacterial meningitis had a normal white cell count.2 Although a result in this case was not available, the findings of Bonsu and Harper emphasise that the full blood count can be normal in children with serious infections. Borschsenius et al suggest that CRP can be valuable in differentiating between meningococcal disease and other diseases.3 However, the fact that in this case the CRP at presentation was less than 10 mg/l suggests this should be exercised with caution.
In conclusion, meningococcal septicaemia can initially be difficult to diagnose. Investigations, in particular CRP, may be normal in the early stages of the disease.
All diagnosis depends on a combination of three processes; history with examination, investigation, and observation. At each stage anxieties may be raised or reduced. Results from investigations should be used to complement the clinical findings rather than replace assessment and re-evaluation of the patient.
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