Peripartum cardiomyopathy (PPCM) is a rare but serious form of cardiac failure affecting women in the last months of pregnancy or early puerperium. Clinical presentation of PPCM is similar to that of systolic heart failure from any cause, and it can sometimes be complicated by a high incidence of thromboembolism. Prior to the availability of echocardiography, diagnosis was based only on clinical findings. Recently, inclusion of echocardiography has made diagnosis of PPCM easier and more accurate. Its etiopathogenesis is still poorly understood, but recent evidence supports inflammation, viral infection and autoimmunity as the leading causative hypotheses. Prompt recognition with institution of intensive treatment by a multidisciplinary team is a prerequisite for improved outcome. Conventional treatment consists of diuretics, β blockers, vasodilators, and sometimes digoxin and anticoagulants, usually in combination. In resistant cases, newer therapeutic modalities such as immunomodulation, immunoglobulin and immunosuppression may be considered. Cardiac transplantation may be necessary in patients not responding to conventional and newer therapeutic strategies. The role of the anesthesiologist is important in perioperative and intensive care management. Prognosis is highly related to reversal of ventricular dysfunction. Compared to historically higher mortality rates, recent reports describe better outcome, probably because of advances in medical care. Based on current information, future pregnancy is usually not recommended in patients who fail to recover heart function. This article aims to provide a comprehensive updated review of PPCM covering etiopathogeneses, clinical presentation and diagnosis, as well as pharmacological, perioperative and intensive care management and prognosis, while stressing areas that require further research.

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Peripartum cardiomyopathy (PPCM) is a rare entity, and anesthetic management for cesarean section of a patient with this condition can be challenging. We hereby present the anesthetic management of a patient with PPCM complicated with preeclampsia scheduled for cesarean section, along with a mini review of literature. A 24 year-old primigravida with twin gestation was admitted to our hospital with severe PPCM and preeclampsia for peripartum care, which finally required a cesarean section. Preoperative optimization was done according to the goal of managing left ventricular failure. Combined spinal epidural (CSE) anaesthesia with bupivacaine and sufentanil was used for cesarean section under optimal monitoring. The surgery was completed without event or complication. Postoperative pain relief was adequate and patient required only one epidural top up with sufentanil 6 hours after operation. To the best of our knowledge there is no report in literature of the use of sufentanil as a neuraxial opioid in the anesthetic management of cesarean section in a patient with PPCM. CSE with sufentanil may be a safer and more effective alternative in such cases.

Propofol-based anesthesia was associated with significantly less postoperative vomiting and faster recovery compared to standard anesthesia in patients undergoing gynecological laparoscopy.

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Enteral feeding is now standard and routine practice in intensive care. The use of a nasogastric tube for enteral feeding is generally considered to be safe, but tubes with small bores can sometimes lead to aspiration or passage clogging when malpositioned in sedated patients who are on long-term mechanical ventilation. Thus, accurate confirmation of correct placement is mandatory in such patients. This is not always the case, but this faulty practice can lead to serious complications in the absence of potential bezoar-forming medicines or gastrointestinal pathology. We present here one such interesting case of a patient who developed esophageal bezoar due to a malpositioned nasogastric tube for administering a casein-containing feed. In addition, we present a review of the literature.

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Pneumonia due to H1N1 infection is now very common. We report a case of ischemic stroke which arose subsequently to H1N1 influenza. The patient was a female who developed acute respiratory distress syndrome (ARDS) after H1N1 influenza, was ventilated as per standard protocol and started treatment with oseltamivir. When sedation was stopped during weaning from the ventilator, she was found to have left hemiparesis resulting from multiple infarctions in the brain. Contrary to thrombocytosis usually seen in acute influenza, the platelet counts in our patient actually dropped. We suspected that increased interleukin release or stickiness of the platelets might have caused this ischemic stroke. In the course of time, she had acceptable neurological recovery following treatment with aspirin and neuro-rehabilitation. This case report provides evidence that a rare, debilitating complication like stroke can occur in H1N1 infection. A high index of suspicion of the probability of a cerebrovascular event should be borne in mind and regular neurological assessment should be done in such cases.