Graves' disease (GD) may display uncommon manifestations. We report a patient with rare complications of GD and present a comprehensive literature review. A 35-year-old woman presented with a two-week history of dyspnea, palpitations, and edema. She had a raised jugular venous pressure, goiter, and exophthalmos. Laboratory tests showed pancytopenia, a raised alkaline phosphatase level, hyperbilirubinemia (mainly direct bilirubin), and hyperthyroidism [TSH: <0.01 mIU/L (reference values: 0.45–4.5), fT4: 54.69 pmol/L (reference values: 9.0–20.0), and fT3: >46.08 pmol/L (reference values: 2.6–5.7)]. Her thyroid uptake scan indicated GD. Echocardiography showed a high right ventricular systolic pressure: 60.16 mmHg. Lugol's iodine, propranolol, cholestyramine, and dexamethasone were initiated. Hematologic investigations uncovered no reason for the pancytopenia; therefore, carbimazole was started. Workup for hepatic impairment and pulmonary hypertension (PH) was negative. The patient became euthyroid after 3 months. Leukocyte and platelet counts and bilirubin levels normalized, and her hemoglobin and alkaline phosphatase levels and right ventricular systolic pressure (52.64 mmHg) improved. This is the first reported single case of GD with the following three rare manifestations: pancytopenia, cholestatic liver injury, and PH with right-sided heart failure. With antithyroid drugs treatment, pancytopenia should resolve with euthyroidism, but PH and liver injury may take several months to resolve.

Introduction: Pain is a very common reason for presenting to the Emergency Department (ED). While the causes for pain are diverse, ranging from fractures and other injuries to chest or abdominal pain or headache, the provision of effective, timely analgesia should be one of the principal goals of emergency staff . Inadequate pain relief and poor treatment in pain management in ED was highlighted by Wilson and Pendleton and they coined the term oligoanalgesia to describe this phenomenon. They found that only 44% of patients with pain received analgesics in the ED, and sub therapeutic dosing was common. Methods: This was a prospective observational study conducted in HGH ED after approval from Department of Emergency Medicine Audit & Ethical Committee, investigators were divided over shifts in ED for 2 weeks. Total of 448 patients were recruited. Inclusion criteria were any patient presented to Ed in acute pain over the last 24 hour, age >18 years old. Patients in life threatening conditions, major trauma, altered mental status or communication difficulties were excluded. Results: Total of 448 patients were recruited. Of which 358 number were males, 90 Number were females. Trauma-related cases composed about 100 number (22.3%) of the pain cases. The number of pain medications prescribed to patients throughout the ED course and upon discharge was recorded. Conclusion: The administration of pain-relieving medications in the ED was associated with significant pain reduction upon disposition. However, pain was still inadequately treated and scoring was not adequately recorded in patient files. Need for proper structured approach for pain management in HGH ED is warranted.

Introduction: The mechanism for carbamate toxicity is reversible cholinesterase inhibition, which leads to accumulation of acetylcholine at the neuromuscular junction.1 The cardiac manifestations of carbamate toxicity are rare. We report a case of carbamate toxicity with atrial fibrillation as the cardiac manifestation. Case presentation: A 28-year-old patient, previously healthy, presented to the ED complaining of diplopia, dizziness, palpitation, and one episode of vomiting. The symptoms began two hours before when he was spraying pesticide at a farm. According to the patient he sprayed 9 liters of pesticide over a short period of two hours. The patient was not using any personal protective equipment. The pesticide used was later identified as Lannate, which contain Methomyl (carbamate). On examination, a chemical odor was noted. His initial vital signs were normal except heart rate of 134/min. The patient was decontaminated in the decontamination room to avoid further exposure. He had constricted pupils of 2 mm. There were no other signs of organophosphate or carbamate toxicity. His initial ECG showed atrial fibrillation (AF) with fast ventricular response rate. The pseudo-cholinesterase level was. The toxicology service was consulted, and they advised not to start antidote treatment only for the AF, as other signs and symptoms were absent. The cardiology on call assessed the patient and started amiodarone infusion presuming new onset of AF. The patient's rhythm reverted back to sinus 12-hour post-presentation. He was discharged next day with a diagnosis of paroxysmal AF secondary to carbamate poisoning. Discussion: AF in carbamate toxicity is rare and only few cases have been reported in the literature.2,3 It is postulated that, enhanced nicotinic activity stimulates postganglionic sympathetic terminals and produces a dramatic release of norepinephrine.4 Norepinephrine mediates its arrhythmogenic effects by increasing automaticity of cardiac cells and by decreasing the cardiac muscle fibrillatory threshold.5