Chin Wang Hsu

Adrenal insufficiency caused by primary aggressive non-Hodgkin's lymphoma of bilateral adrenal glands: report of a case and literature review

Abstract A 64-year-old woman was hospitalized because of poor general condition, gastrointestinal upset, unexplained fever, electrolyte imbalances, and an incidental finding of bilateral huge adrenal masses on computerized tomography (CT) of the abdomen. Non-Hodgkins lymphoma (NHL) of B-cell origin was proven by ultrasound-guided aspiration biopsy of the left adrenal gland. Meanwhile, primary adrenal insufficiency was confirmed by her low serum cortisol level, high ACTH level, and inadequate adrenal response to the rapid ACTH stimulation test. The diagnosis of primary adrenal NHL was supported by detailed physical examinations, bone marrow examination, and such imaging studies as CT scan and sonography. She received three courses of chemotherapy with cyclophosphamide, vincristine, and prednisolone and there was an initial transient response, but she died of sepsis and progression of NHL three and a half months later.

A Simple and Rapid Approach to Hypokalemic Paralysis

Hypokalemia with paralysis (HP) is a potentially reversible medical emergency. It is primarily the result of either hypokalemic periodic paralysis (HPP) caused by an enhanced shift of potassium (K(+)) into cells or non-HPP resulting from excessive K(+) loss. Failure to make a distinction between HPP and non-HPP could lead to improper management. The use of spot urine for K(+) excretion rate and evaluation of blood acid-base status could be clinically beneficial in the diagnosis and management. A very low rate of K(+) excretion coupled with the absence of a metabolic acid-base disorder suggests HPP, whereas a high rate of K(+) excretion accompanied by either metabolic alkalosis or metabolic acidosis favors non-HPP. The therapy of HPP requires only small doses of potassium chloride (KCl) to avoid rebound hyperkalemia. In contrast, higher doses of KCl should be administered to replete the large K(+) deficiency in non-HPP.

Risk Factors for Recurrent Hypoglycemia in Hospitalized Diabetic Patients Admitted for Severe Hypoglycemia

Purpose Severe hypoglycemia can result in neural damage, impaired cognitive function, coma, seizures, or death. The decision to admit diabetic patients after initial treatment in the emergency department remains unclear. Our purpose is to identify risk factors for developing recurrent hypoglycemia in diabetic patients admitted for severe hypoglycemia. Materials and Methods We reviewed the records of 233 subjects (92 males, 141 females; mean age, 74.1 ± 9.8 years) with type 2 diabetes treated at a tertiary care teaching hospital and hospitalized for severe hypoglycemia. Results Seventy-four (31.8%) patients were categorized with recurrent hypoglycemia and 159 (68.2%) with non-recurrent. Multivariate logistic regression analysis revealed that patients with loss of a recent meal, coronary artery disease, infection, and poor renal function (lower estimated glomerular filtration rate) were at risk for recurrent hypoglycemia. The use of calcium-channel blockers appeared to be a protective factor for the development of recurrent hypoglycemia. Conclusion There may be a subset of patients with severe hypoglycemia and certain risk factors for recurrent hypoglycemia that should be admitted.

Intraventricular hematoma, subarachnoid hematoma and spinal epidural hematoma caused by lumbar puncture: an unusual complication.

Lumbar puncture is a commonly practiced bedside technique for acquiring cerebrospinal fluid for the purposes of examination, spinal anesthesia, and as therapeutic trial for normal pressure hydrocephalus. Headache and backache after lumbar puncture are not uncommon. We report an elderly woman who suffered from altered consciousness and acute neurologic deficit after a difficult lumbar puncture. Serial imaging studies revealed active bleeding from the left first lumbar artery with the formation of spinal epidural hematoma and coexisting acute cranial intraventricular hematoma and subarachnoid hemorrhage. Lumbar puncture may rarely associate with life-threatening complications. Acute spinal subdural hemorrhage or subarachnoid hemorrhage after lumbar puncture is a timely diagnosis and needs urgent interventions. Clinicians should be aware of these rare but life-threatening complications after lumbar puncture. A cranial unenhanced CT is mandatory for patients having acute altered consciousness after lumbar puncture. A thorough vascular imaging evaluation from the lumbar spine to the brain is warranted in selected cases.

Movement disorder caused by abuse of veterinary anesthesia containing tiletamine

Zoletil (Telazol) is a fixed-ratio combination of the tranquilizer zolazepam, with the dissociative anesthetic tiletamine, used for injection anesthesia in dogs, cats, wild, and zoo animals. We report a veterinarian who developed movement disorder after abuse of Zoletil for a 2-week period. Phencyclidine derivatives, that is, tiletamine can induce movement disorder in human. Tiletamine/zolazepam can be abused for recreational purpose, especially by those people with easy access to veterinary medications. Emergency physicians should have high alert to the diverse presentations of drug abuse. This case again highlights that the association between accessibility of scheduled drugs and health care professionals.

Hypoglycemia revisited in the acute care setting

Hypoglycemia is a common finding in both daily clinical practice and acute care settings. The causes of severe hypoglycemia (SH) are multi-factorial and the major etiologies are iatrogenic, infectious diseases with sepsis and tumor or autoimmune diseases. With the advent of aggressive lowering of HbA1c values to achieve optimal glycemic control, patients are at increased risk of hypoglycemic episodes. Iatrogenic hypoglycemia can cause recurrent morbidity, sometime irreversible neurologic complications and even death, and further preclude maintenance of euglycemia over a lifetime of diabetes. Recent studies have shown that hypoglycemia is associated with adverse outcomes in many acute illnesses. In addition, hypoglycemia is associated with increased mortality among elderly and non-diabetic hospitalized patients. Clinicians should have high clinical suspicion of subtle symptoms of hypoglycemia and provide prompt treatment. Clinicians should know that hypoglycemia is associated with considerable adverse outcomes in many acute critical illnesses. In order to reduce hypoglycemia-associated morbidity and mortality, timely health education programs and close monitoring should be applied to those diabetic patients presenting to the Emergency Department with SH. ED disposition strategies should be further validated and justified to achieve balance between the benefits of euglycemia and the risks of SH. We discuss relevant issues regarding hypoglycemia in emergency and critical care settings.

Hyperacute cerebral fat embolism in a patient with femoral shaft fracture

Fat embolism syndrome is a potentially fatal complication and occurs most commonly after long bone fracture. In patients who sustained severe trauma, both cerebral fat embolism(CFE) and diffuse axonal injury (DAI) could be the cause of altered consciousness in the absence of marked intracranial lesions in cranial computed tomography. However, distinguishing CFE and DAI can be difficult clinically. Generally, DAI develops immediately after the insult, whereas CFE occurs 48 to 72 hours after the trauma and even after internal fixation for the fractures. Fat embolism syndrome develops within an average of 48.5 hours after long bone fracture [1] but has never been reported to occur in less than 2 hours. Here, we present a patient who developed hyperacute CFE and eventually had poor neurological outcome, in contrast to previous reports stating that CFE usually has a long latent period and favorable outcomes.

Syncope as the Sole Manifestation of Acute Right Ventricular Myocardial Infarction in a Non-Diabetic Patient

Syncope is a symptom defined as a transient, self-limited loss of consciousness, usually leading to a fall. The causes of syncope are numerous, but life-threatening conditions should be identified as the first priority in order to avoid a catastrophic outcome. Here we report a non-diabetic patient who presented syncope as the sole manifestation of a silent acute right ventricular myocardial infarction (RVMI). The cause of syncope in this patient was assumed to be hypoperfusion of sinus node artery arising from the right coronary artery, hence causing transient sinus node dysfunction. Syncope could be the sole manifestation of RVMI complicated with sinus node dysfunction. Lead Ⅱ in ECG monitoring itself could only provide limited information and a panel of 12-lead ECG is required in all patients presenting with syncope, even in the absence of typical symptoms of acute coronary syndrome or hemodynamic instability. Continuous ECG monitoring and prolonged ED observation in a syncopal patient without immediately identifiable causes is warrant to avoid such potentially life-threatening condition.

Acute Aortic Dissection Presenting with Acute Lower-back Pain Following Sexual Intercourse

Acute aortic dissection, an emergent vascular catastrophe, varies in its clinical presentation and embraces a high mortality rate if not recognized early. Here we report a 32-year-old man who presented to our emergency department (ED) because of lower-back pain shortly before orgasm, and was subsequently found to have retrograde acute type B aortic dissection. This young man was diagnosed and treated promptly in the ED and had no sequelae. We highlight that ED physicians should always include vascular emergencies (i.e. acute aortic dissection) in their differential diagnoses whilst engaging a patient with an acute-onset severe lower-back pain featuring a characteristic upward propagation that emerges following strenuous exercise (i.e. sexual intercourse) in our case. This would appear to be especially so for patients featuring elevated blood pressure regardless of patients age or history of hypertension.