BackgroundPatients with adrenal insufficiency (AI) have excess mortality, in part due to the occurrence of life‐threatening adrenal crises. Infective processes, including that of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), are recognised as the major precipitant of adrenal crises. Adverse reactions to the ChAdOx1 SARS‐CoV‐2 vaccine occur in a significant proportion of individuals, however, are mild‐moderate in the majority of cases.DesignCase series.Patients & ResultsWe describe five cases where more severe adverse reactions to the ChAdOx1 SARS‐CoV‐2 vaccine led to actual or incipient adrenal crises requiring parenteral hydrocortisone within 24 h of receiving the first ChAdOx1 SARS‐CoV‐2 vaccination.ConclusionIn individuals with adrenal insufficiency, adverse reactions to the initial dose of the ChAdOx1 SARS‐CoV‐2 vaccination can precipitate adrenal crises. We recommend that patients with AI should immediately increase their maintenance glucocorticoid dosage 2–3 fold on experiencing any symptoms in the initial 24 h following vaccination.
Summary:A previously fit 56 year old female presented with a rapidly progressive and fatal pneumococcal septicaemia with disseminated intravascular coagulation. Post-mortem studies confirmed a Waterhouse-Friderichsen syndrome and revealed an anatomically normal spleen; intracellular diplococci were seen within splenic macrophages providing evidence of normal splenic function. This appears to be only the second case of Waterhouse-Friderichsen syndrome due to pneumococcal septicaemia in a patient with a normal spleen.
A 56-year-old woman with a medical history of hypertension presented to our hospital with back pain, abdominal pain, vomiting and elevated blood pressure. The laboratory parameters including evaluation for secondary hypertension were within normal ranges at the time of presentation. During her hospitalisation, fluctuations in her blood pressure and pulse were observed which were attributed to autonomic disturbances, the cause of which was unknown. On the seventh day after presentation to the hospital, the patient developed focal seizures and slurred speech which was believed to be secondary to hyponatraemia detected at that time. Hyponatraemia improved with hypertonic saline and she experienced no further seizures. On the eighth day of her admission, she developed acute flaccid paralysis of all her limbs and respiratory distress. We concluded this to be secondary to Guillain-Barre syndrome (GBS). She responded to plasmapheresis.The presence of dysautonomia and hyponatraemia before the onset of paralysis makes this a rare presentation of GBS.
We read with interest the article by Baiges et al., (1) which shed light on the rare entity of the Abernethy malformation and gives a working algorithm for extrahepatic shunts. We commend all the researchers for the effort to put together a large series and have a follow-up up to the age of 30 years, missed by previous series.The researchers have shown how shunt closure can be considered in therapeutic and prophylactic settings to reduce complications. However, the researchers have not given us details on the precise anatomy of the shunts they saw in the series. This is important in planning an intervention.The Abernethy malformation is commonly described as the shunting of splanchnic blood into the systemic venous network by abnormal communications. The Abernethy malformation is anatomically classified as a type 1 (Ia)-splenic and superior mesenteric vein draining separately in the inferior vena cava (IVC) and (Ib) draining though a common trunk. Type 2 is classified as a shunt from the portal vein (PV) to IVC. (1,2) The Kobayashi classification describes types A, B, and C of portal blood flowing directly into the IVC, renal vein, and iliac vein, respectively. Blanc et al. classified the congenital extrahepatic portosystemic shunt considering the starting as well as the end point of the shunt. (2,3) Based on our clinical observations, we believe the Abernathy malformation can also result in, portal blood being shunted directly into the right atrium (RA), although has not been described in any of the previous classifications. Hence, we believe this is a description of a porta-atrial shunt. This should perhaps be incorporated into the current classifications, and also also provides an opportunity to further understand hepatic vascular embryology, malformations, and their clinical spectrum. Moreover, such large shunts with direct communication with the RA may not be amenable to the usual radiological interventions.
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