No abstract

Malnutrition commonly complicates the course of patients with cirrhosis and has a multifactorial etiology. Despite the important role that nutrition plays in the prognosis of those with cirrhosis, the nutrition assessment process can be challenging in this setting. A number of tools are available to aid in the nutrition assessment of the cirrhotic patient; however, none are without limitations. Although the assessment process can be difficult, the ability to properly manage the nutrient needs of the patient presents an additional set of challenges because of the catabolic nature of the disease process and common occurrence of anorexia and other symptoms leading to poor oral intake. In this review, the nutrition assessment tools and general guidelines for nutrition management in patients with advanced liver disease are discussed to promote recognition of the nutrition issues affecting this patient population and lead to their improved survival and reduced morbidity.

A ventricular assist device (VAD) is an implantable mechanical device that is used to partially or completely replace the circulatory function of a failing heart. VADs may serve as a bridge to heart transplantation or as permanent circulatory assistance, also referred to as destination therapy. There is a paucity of information regarding the nutrition complications in VAD patients, and as such, little is presently known of the optimal means of nutrition assessment and management of these complex and often critically ill patients. In this review, a general overview of the VAD, comparisons of nutrition assessment measures, and strategies to meet the nutrition needs of these patients are provided using evidence-based information wherever possible. Because there is a lack of nutrition studies and assessment guidelines specifically for VAD patients, many of the guidelines for care of these patients are currently based on the information available for the care of patients with heart failure. Although the optimal measure to assess nutrition status remains poorly studied, a systematic, thorough nutrition assessment of patients with heart failure and heart transplant candidates prior to VAD placement appears to be important to identify those at nutrition risk and, with appropriate nutrition therapy, decrease their risk for morbidity and mortality. VAD patients with inadequate oral intake may require nutrition support to meet their nutrition needs; however, feeding the hemodynamically compromised patient provides additional challenges.

haemolysis associated with ALP poisoning is very rare, reported previously in only two cases in the literature.3 4 Herein, we report a patient with ALP poisoning presenting with intravascular haemolysis secondary to G6PD deficiency.A 22-year-old man presented to the emergency department with nausea, epigastric distress, vomiting and cola-coloured urine after intentional ingestion of one tablet of ALP. He denied taking any other drug or intoxicant. On admission, he was fully conscious, icteric, normotensive, with mild tachycardia. His breath had a strong garlic odour. The rest of the physical examination was unremarkable. The urine sample obtained was deep brown. The electrocardiogram showed only sinus tachycardia. Arterial blood gases and renal functions were normal. His liver-function tests showed unconjugated hyperbilirubinaemia with no transaminitis, and normal alkaline phosphatase. A peripheral smear obtained showed spherocytes, Heinz bodies and occasional degmacytes. The plasma haemoglobin level was raised at 64 mg/dl and the corresponding urine haemoglobin level was 12 mg/ dl. Ultrasound examination of the abdomen showed normal hepatobiliary system and mild splenomegaly. A G6PD assay obtained at presentation showed deficient activity. He was managed with Ryle's tube lavage, aggressive fluid rehydration, sodium bicarbonate and magnesium sulphate. He improved clinically (bilirubin decreased from 9.8 to 4.2 mg/dl) and was discharged after a psychiatric evaluation, family screening and appropriate advice regarding G6PD deficiency.ALP is a solid fumigant pesticide which acts by liberating phosphine gas (an oxidant), and thus can cause haemolysis in persons with G6PD deficiency.3 4 ALP by itself can cause haemolysis 4 and also secondary to metabolic acidosis related to hypotension, cardiogenic shock, renal failure, seizures and hepatotoxicity. Haemolysis in ALP poisoning is rare despite the common presence of G6PD deficiency, possibly owing to cardiogenic shock and death supervening before clinically evident haemolysis; mild haemolysis is missed in the face of overwhelming systemic toxicity and the presence of less severe variants of G6PD in northern India, where ALP poisoning is common. 1 In conclusion, although haemolysis is a rare presentation in ALP poisoning, detection of associated G6PD deficiency is imperative because of its attendant implications. R Srinivas, R Agarwal