Neuroleptic Malignant Syndrome (NMS) after Treatment with Metoclopramide - A Rare Case Report

Neuroleptic Malignant Syndrome (NMS) is a medical emergency. It presents with mental status change, rigidity, fever, and autonomic dysfunction. It is caused by antipsychotics especially neuroleptic agents and certain antiemetic drugs like metoclopramide that block central dopamine pathways. We present a case of a 32-year-old male chronic alcoholic who presented to us with alcohol withdrawal symptoms and was given injection metoclopramide and developed neuroleptic malignant syndrome (NMS).Incidence rates for NMS range from 0.02 to 3 percent in patients treated with antipsychotic agents.1,2 Though it is commonly encountered in young adults, any age group can be affected.3,4 Males are two-fold more affected than females.4Metoclopramide, a commonly used anti-emetic agent has anti-dopaminergic properties and can give rise to development of NMS. The signs and symptoms of NMS include hyperthermia, altered mental status, muscular rigidity resembling extrapyramidal rigidity, autonomic instability, diaphoresis, hyper salivation, dysphagia, tachycardia, hypertension. NMS if left untreated, is usually fatal. So, early recognition and treatment is of great importance.

Acute Transient Hemiparesis - An Unusual Pseudo Exacerbation of Multiple Sclerosis

Multiple sclerosis is a chronic demyelinating disease characterised by inflammation and plaque formation. Multiple sclerosis has many variants. It presents as four clinical forms, Relapsing Remitting Multiple Sclerosis (RRMS), Primary Progressive Multiple Sclerosis (PPMS), and Secondary Progressive Multiple Sclerosis (SPMS) and Primary Relapsing Multiple Sclerosis (PRMS). RRMS can present as acute attacks. They should be differentiated from pseudo-exacerbations. True exacerbation is when a new lesion appears in the brain or spinal cord, with a neurological episode lasting for more than 24 hours, with a period of clinical stability over the last 30 days.1 Any flaring up of symptoms of multiple sclerosis due to external factors such as fever, heat or infection is called pseudo-exacerbations. Pseudo-exacerbation episodes do not last for more than 24 hours and should resolve with treatment of the underlying fever or infection.2

Subdural Haematoma (SDH) Leading to Subfalcine Herniation in a Case of End Stage Renal Disease

Subdural haematoma (SDH) is characterized by bleeding into the sub dural space surrounding the brain. It is mostly associated with atraumatic brain injury. It usually results from tears in bridging veins that cross the subdural space. ESRD is a risk factor for SDH. Coagulation abnormalities, volume overload, haemodialysis and platelet dysfunction predispose to SDH in ESRD and increase the morbidity and mortality.1 We report a case of a 44-year-old female, a known case of chronic kidney disease on maintenance haemodialysis who developed SDH with resulting subfalcine herniation.

Atypical Presentation of Gitelman Syndrome (GS) Masquerading as Hypokalaemic Periodic Paralysis

Gitelman syndrome once considered to be a subset of Barter’s syndrome, is a disorder of the distal tubule.1,2 It is an inherited disorder of the thiazide sensitive sodium-chloride transport channel. It is characterised by its main clinical features of metabolic alkalosis, hypomagnesemia, hypokalaemia and hypocalciuria. It’s an infrequently diagnosed condition where there diagnosis is made based on the clinical and the biochemical parameters of the disease. We present a case of Gitelman syndrome in a young male who presented with recurrent episodes of weakness to different private hospitals with documented hypokalaemia and labelled as hypokalaemic periodic palsy (HPP), presented to us with quadriparesis and on investigation diagnosed as GS.

Methotrexate (MTX) Induced Pancytopenia - A Rare Serious Adverse Effect

A 65-year-old woman presented to us with complaints of fatigability and appearance of red spots on extremities since 6 days. She was a known case of rheumatoid arthritis since 5 years and was on tablet prednisolone 5 mg OD and tablet hydroxychloroquine 200 mg bid orally. Two months back she had exaggerated symptoms in the form of increased joint pains for which tablet methotrexate 7.5 mg was started weekly once and was increased to 7.5 mg bid (15 mg) per week 2 weeks back along with folic acid 5 mg per day.Methotrexate (MTX) is a folate antagonist used to treat various malignancies, and autoimmune disorders including rheumatoid arthritis. It enters cell by an active cellular uptake and inhibits dihydrofolate reductase (DHFR) enzyme that converts dihydrofolate (DHF) to tetrahydrofolate (THF) affecting purine and ultimately DNA synthesis. Cell with capability of polyglutamylation like myeloblasts and lymphoblasts are most susceptible to the effects of MTX because polyglutamylation prolongs its intracellular presence.1,2

Clinical Application of Fasting and Post-Prandial Lipid Profile in Patients of Chronic Kidney Disease.

Dyslipidemia is a traditional risk factor for cerebrovascular disease and cardiovascular disease (CVD). CKD is associated with dyslipidemia. Patients with CKD will be more prone to the CVD and cerebrovascular disease as compared to normal healthy individuals. Thus, it is important to cover the postprandial lipid profile for better assessment and treatment of dyslipidemia. We wanted to study the postprandial lipid profile in patients of CKD. MethodsThis is a case control study conducted in Acharya Vinoba Bhave Rural Hospital (AVBRH) Sawangi (Meghe), Wardha, Maharashtra, between September 2016 and September 2018. In this study, we enrolled 150 cases and 75 controls. ResultsFasting lipid profile in CKD patients was higher as compared to controls and was found to have similar post-prandial lipid profile. When we compared the fasting and post-prandial lipid profile in patients with CKD, we found that a substantial difference existed. We found a considerable difference in the fasting and post-prandial lipid profiles even in the controls. ConclusionsPatients with CKD and diabetes mellitus had a significant increase in the total cholesterol, triglycerides, low density lipoprotein and very low-density lipoprotein in the fasting and post-prandial state. In clinical practice, the implementation of standardized methodologies and biomarker profiles would allow for the early and reliable detection of those at risk.

Splenic Abscess Complicating Scrub Typhus Induced Splenic Infarct - A Rare Case Report

Any condition leading to the interruption of blood flow to the spleen, such as blockage in the splenic artery due to a plaque or a clot in one of its branches leads to Splenic Infarction. It could also be due to infection, trauma, disseminated intravascular coagulation and vasculitis. The complications of splenic Infarct include pseudocyst, haemorrhage, rupture, aneurysm and rarely abscess formation due to infection of the infarcted region. Splenic abscess is a rare and potentially lethal clinical condition. We present a case of a 24-year-old male who was diagnosed with splenic infarct because of scrub typhus and later developed splenic abscess.Spleen is a lymphatic organ present in the left hypochondrium of the abdomen. It filters and stores the red cells, produces white blood cells and scavenges microorganisms like bacteria. Any condition leading to the interruption of blood flow to the spleen could cause an infarct. The infarction could be classified as partial or complete based on the extent of involvement. The area of the spleen which had loss of blood supply leading to the death of the area is called splenic Infarct. It could also be due to infection, trauma or certain diseases. Rarely splenic infarcts may lead to formation of abscess. The most commonly occurring symptoms of a splenic abscess pain in the abdomen, fever and nausea are not specific to splenic abscess.[1] Hematogenous spread is the most common cause of splenic abscess.[2]

Acute Exacerbation of COPD Triggered by Pneumonia, and Secondary Spontaneous Pneumothorax (SSP).

Secondary Spontaneous Pneumothorax (SSP) can rarely complicate Chronic Obstructive Pulmonary Disease (COPD). Infections are common triggers for exacerbations of COPD. COPD with acute exacerbation presents with increasing dyspnoea. We present a rare case of a 75 year old female, who was a known case of COPD and developed right middle lobe pneumonia with partial collapse of the middle lobe along with a secondary spontaneous pneumothorax.

Hashimoto s Encephalopathy (HE) - Early Manifestation of Impending Thyroid Storm.

Dear Dear HyperthyroidismiHyHyperthyroidism may be associated with various neuropsychiatric manifestations like anxiety, irritability, restlessness, decrease in concentration, dementia, lack of judgement and planning.[1] Rarely, seizures, myoclonus, chorea, or catatonia can occur. Encephalopathy may be present in only 1% of cases.

Sporadic Liddle s Syndrome

Liddle's syndrome is a classical entity which rarely presents with secondaryhypertension. Work up for this entity is necessary while dealing with cases ofhypertension, because the treatment protocol is different. We report a case of a 35-year-old male, who presented to us with history of recurrent headaches andfatiguability. Examination revealed hypertension and hypokalaemia. No one in familywas hypertensive. After work up, he was diagnosed to have Liddle’s syndrome.Liddle's syndrome is inherited as an autosomal dominant condition. It ischaracterized by increased sodium reabsorption and potassium secretion bykidneys.[1-3] The classic triad of presentation is hypertension, hypokalaemia, andmetabolic alkalosis, which often resembles hyperaldosteronism.[4] It usually affectsyounger age group,, but rarely it may be diagnosed in adulthood.[5]Secondary hypertension may be the first presentation in Liddle’s syndrome.Diagnosis of this syndrome is important because the treatment is different from thatof other causes of secondary hypertension. The triad of hypertension, hypokalaemiaand metabolic alkalosis is usually seen in Liddle’s syndrome.

Acute Liver Failure and Intravascular Haemolysis in Zinc Phosphide Poisoning.

A 37-year-old male presented with symptoms of nausea, vomiting, abdominal pain, jaundice, lacrimation and reddish brown urine discoloration since 2 hours after ingestion of 30 gms of zinc phosphide with suicidal intent 4 hours before arriving at the hospital. There was no history of hematemesis, melena, convulsions. On examination blood pressure: 140/90 mmHg, Pulse: 120 beat per minute, RR: 24 cycles/minute, temperature: 37.5°C and O2 saturation: 91 percent in room air. Visible icterus was present. Diffuse tenderness was reviled by abdominal tests. Organomegaly was not present. The neurological examination was not important. There were flapping tremors. With 0.9 percentage of NaCl solution added with activated charcoal, the patient was given gastric lavage. Table 1 displays laboratory tests in the emergency department.

Mixed Connective Tissue Disease Presenting As Quadriparesis In A Female

Mixed connective tissue disease (MCTD), or overlap syndrome, is a multisystem autoimmune disease characterized by a combination of clinical features similar to those of polymyositis, systemic sclerosis, and rheumatoid arthritis. MCTD patients present with a distinct rise (high titers) of anti-U1 ribonucleoprotein antibody in serum. Here, we present the case of a 45-year-old female who presented with subacute onset weakness on all four limbs and later on diagnosed as overlap syndrome with severe myositis