CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 2, May/June 2023 118 AFRICA kidney injury with hyperkalaemia, metabolic acidosis and the liver enzymes were elevated. Resuscitation was commenced with intravenous fluids, inotropes and blood products, and a cephalosporin antibiotic was started. Diphtheria antitoxin was not immediately available. Tracheostomy and dialysis were planned. However, shortly after arrival in ICU, the patient complicated with a ventricular tachycardia, which rapidly progressed to ventricular fibrillation. Defibrillation and cardiopulmonary resuscitation were unsuccessful. Post mortem findings confirmed multi-organ involvement with fulminant systemic diphtheria. Grossly, there was a bull neck with swelling/oedema of the oropharyngeal soft tissue. The tonsils, pharynx, pharyngeal lymph nodes and epiglottis showed an inflammatory cell infiltrate with necrosis, pseudomembrane formation and bacterial colonies. The enlarged pharygeal lymph nodes demonstrated suppurative inflammation and necrosis. The heart demonstrated myocarditis with myocytolysis and lipid accumulation. Dissection of the conducting system demonstrated lipid accumulation, lymphocytic infiltration and myocyte necrosis (Fig. 3A, B). The renal changes were consistent with acute tubular necrosis (Fig. 4A). Cutaneous ulceration in the foot showed a superficial exudate, which was confirmed to be toxin-producing Corynebacterium diphtheria (Fig. 4B). Microbiological and molecular investigation of the tonsils and skin ulcer confirmed C diphtheria, culture positive, biotype mitis, toxin producing.4 Discussion Despite receiving appropriate immunisations until two years of age, this patient developed an aggressive diphtheritic infection complicated bymyocarditis, acute kidney injury and disseminated intravascular coagulopathy. Table 1. Laboratory results Full blood count Hb 9.6 g/dl, WCC 19.7 × 109 cells/l, platelets 22 × 109 cells/l Blood smear Neutrophilia, left shift with toxic granulation, marked thrombocytopaenia, red cell fragmentation C-reactive protein 89 mg/l (normal 0–5 mg/l) Procalcitonin 7.38 ng/ml (normal < 0.5 ng/ml) Electrolytes Na 142 mmol/l, K 5.4 mmol/l, Cl 115 mmol/l, HCO3 14 mmol/l, urea 59 mmol/l, creatinine 595 µmol/l CPM Ca 2.13 mmol/l, P 1.86 mmol/l, Mg 1.05 mmol/l Liver function Total protein 32 g/l, albumin 17 g/l, bilirubin 2 µmol/l, ALT 123 U/l, AST 414 U/l, ALP 194 U/l, GGT 14 U/l INR 1.5 Hb, haemoglobin; WCC, white cell count; Na, sodium; K, potassium; Cl, chlorine; HCO3, bicarbonate; Ca, calcium; P, phosphate; Mg, magnesium; ALT, alanine transaminase; AST, aspartate transaminase; ALP, alkaline phosphatase; GGT, gamma glutamyl transferase; INR, international normalised ratio. Fig. 2. Chest radiograph shows new consolidation/collapse of the right upper lobe, presumed to have resulted from dislodgement of the pseudomembrane, with resultant bronchial obstruction. Fig 3A. Diphtheritic myocarditis: the cardiac myocytes show myocytolysis (HE × 40). B. Myocardial involvement showing lipid accumulation (HE × 40). A B
RkJQdWJsaXNoZXIy NDIzNzc=