LAUSR

Cerebral microhemorrhages or CMBs are small, hypointense foci occurring in the brain parenchyma, with a maximum size of 5 mm, or even up to 10 mm on haemorrhage sensitive MRI sequences. Traditionally, this clinical entity is seen in conditions such as cerebral amyloid angiopathy (CAA), chronic hypertension (termed hypertensive microangiopathy), and diffuse axonal injury (seen especially in a history of trauma) – with their own specific patterns on MRI. The advent of technology in MRI has allowed increased utilization of haemorrhage sensitive sequences, namely gradient echo (GRE) and susceptibility weighted imaging (SWI) in routine brain scans. On histopathological examination, these microhemorrhages are due to hemosiderin accumulation in macrophages [1]. The presence of hemosiderin causes the signal loss, or hypointense appearance on GRE/SWI sequences. Despite the increased detection, the clinical significance of microhemorrhages remains controversial – complicating patient management. There is increasing literature available attributing the occurrence of cerebral microhemorrhages to other, less well known causes, such as high-altitude exposure, acute respiratory distress syndrome (ARDS), infective endocarditis, or critical illnesses/sepsis; even so, most of the literature discusses this entity in the adult population. Scarce literature is available describing its occurrence in the pediatric population. Herein, we discuss the occurrence of cerebral microhemorrhages in a pediatric patient with critical illness, in our institution. A 2-year-old, otherwise healthy boy presented with fever, upper respiratory tract symptoms, and rapid breathing for 3 days. No history of trauma was notable. He was born full term, with no significant antenatal or postnatal history. Delivery was via spontaneous vaginal delivery. His immunization was up to date. On examination, he was lethargic looking, with a recorded temperature of 40 °C. He was sitting in a leaning forward position, and was noted to be tachypneic, with a respiratory rate of 50 breaths per minute. Saturation on room air was 94%. Subcostal, as well as intercostal recessions were present. Stridor was evident. His peripheries were cold, however, pulse volume was still good. Blood pressure was 108/84 mmHg. Auscultation of the lungs noted generalized rhonchi and crepitations; the remaining systemic examination was unremarkable. A preliminary diagnosis of epiglottitis was made, with possible airway compromise. The otorhinolaryngology (ORL) and anaesthetic teams were consulted, anticipating the possibility of epiglottitis with difficulty in intubation for airway protection. Direct laryngoscopy revealed an inflamed and swollen epiglottis; the child was subsequently intubated and admitted to the intensive care unit (ICU), for further management. While in the ICU, he developed nosocomial pneumonia and a few episodes of tachycardia and desaturation, requiring multiple rounds of nebulization as well as subcutaneous bricanyl. Intravenous antibiotics were initiated. Cultures were negative, while the blood investigations did not suggest presence of disseminated intravascular coagulopathy. After 1 week of ICU admission, attempts were made to extubate; however, child did not show full Glasgow Coma Scale (GCS) recovery. An urgent cranial computed tomography (CT) was pursued, revealing small, punctate hemorrhages at the left frontal and parietal regions. His clinical condition eventually improved, and was transferred to the general paediatrics ward. Neurological assessment while in the ward noted presence of upper motor neuron signs, which were previously absent. The child had increased deep tendon reflexes, positive Babinski's sign, but absence of superficial reflexes, fasciculations, and atrophy. Daily assessment noted resolution of these signs. He was then discharged well, after a total of 4 weeks of admission, and arranged for a follow up magnetic resonance imaging (MRI) of the brain on an outpatient basis, 6-months post discharge. The brain MRI revealed hypointense foci at the previously noted areas of punctate hemorrhages on CT, as well as numerous other small similar signal foci measuring< 5 mm, distributed juxtaand subcortically, as well as concentrated at the splenium of the corpus callosum [Fig. 1]. These abnormal signals spared the thalami, deep gray matter, and cortex, and were only seen on the GRE sequence. Based on the MRI appearance and pattern, a diagnosis of sepsis/critical illness associated microhemorrhages was made. The child remains under the paediatrics clinic follow up, and shows no recurrence of the upper motor neuron signs seen while he was admitted.