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Alcoholic Ketoacidosis Uptodate

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis Damian Baalmann, 2nd year EM resident A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management? Alcoholic Ketoacidosis (AKA): What is it? Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine. Alcoholic Ketoacidosis: How do I recognize it? Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folk Continue reading >>

Some Thoughts On The Keto Diet

Some Thoughts On The Keto Diet

10 America has a new (old) fad diet. Have you heard of it? The keto diet (short for ketogenic) is a high-fat, adequate-protein, low-carbohydrate diet. It is essentially the Atkins diet of the 2000s, but it dates back to the 1920s, when it was used to treat children with epilepsy. The goal of a keto diet is to get at least 70 percent of your calories from fat, no more than 25 percent of calories from protein and only 5 to 10 percent from carbohydrates. For most people, that means restricting your carbohydrate intake to below 50 grams a day. If you’re a breakfast taco fan like me, two tacos will put you at your daily carbohydrate limit, and don’t even think of putting potatoes in there! Half a cup of roasted potatoes will send you over the 50-gram limit. To further put that number of carbs into perspective, the following contain about 15 grams of carbohydrates: one slice of bread, 1/3 cup of rice, one cup of milk, 15 grapes, half of a large banana and a 12-ounce Bud Light (beers with higher alcohol will most certainly contain much more than 15 grams). The impetus for such a carbohydrate restrictive diet was therapeutic in nature. The diet first started nearly 100 years ago when doctors found that when epileptic children switched to a strict all-fat diet, the brain adapted its fuel source and the children had fewer seizures. The ketogenic diet is used to this day to help treat epilepsy, but over the past year or so, millions of everyday eaters have flocked to it for its purported health weight loss benefits. The goal of this diet is to force the body to burn fat instead of carbohydrates as fuel, which produces ketones. Our body and brain then use these ketones to fuel our cells. The increase in ketones puts the body in ketosis, a natural process the body initiates to h Continue reading >>

Best Case Ever 58 Euglycemic Dka

Best Case Ever 58 Euglycemic Dka

This is EM Cases Best Case Ever 58 – Euglycemic DKA with Walter Himmel, the walking encyclopedia of emergency medicine. It’s not only run of the mill DKA, starvation and alcoholic ketoacidosis that can cause a metabolic acidosis with elevated ketones. Euglycemic DKA can be caused by the newer diabetes medications sodium-glucose co-transporter 2 inhibitors like Canagliflozin; and it’s important to recognize this tricky diagnosis early and initiate treatment for DKA despite a normal serum glucose level, because DKA can lead to serious complications like renal failure, cerebral edema, ARDS, shock, and death. Podcast production, sound design and editing by Anton Helman; Written by Anton Helman, June 2017 Euglycemic DKA can occur in any diabetic and has been reported in the literature since the 1970’s, but there has recently been a rise in incidence of euglycemic DKA associated with sodium-glucose co-transporter 2 inhibitors (SGLT-2 inhibitors, or the “zins”) such as Canagliflozin, Dapagliflozin and Empagliflozin. When to suspect euglycemic DKA Any patient with Type 1 or 2 diabetes taking SGLT-2 inhibitors who presents with nausea, vomiting, SOB or malaise or is found to have a metabolic acidosis should have blood drawn for serum ketones. Triggers of euglycemic DKA are similar to the triggers for any DKA: Alcohol use, infection and reduced oral intake. Distinguishing euglycemic DKA from alcoholic DKA Alcoholic ketoacidosis may also present with nausea, vomiting, malaise, ketones and anion gap metabolic acidosis. The key differentiating factor besides the obvious history of heavy alcohol use vs a diabetic taking an SGLT-2 inhibitor, is that patients with alcoholic ketoacidosis tend to have frankly low glucose. How is treatment of euglycemic DKA different? In addit Continue reading >>

Ketosis Vs. Ketoacidosis: What You Should Know

Ketosis Vs. Ketoacidosis: What You Should Know

Despite the similarity in name, ketosis and ketoacidosis are two different things. Ketoacidosis refers to diabetic ketoacidosis (DKA) and is a complication of type 1 diabetes mellitus. It’s a life-threatening condition resulting from dangerously high levels of ketones and blood sugar. This combination makes your blood too acidic, which can change the normal functioning of internal organs like your liver and kidneys. It’s critical that you get prompt treatment. DKA can occur very quickly. It may develop in less than 24 hours. It mostly occurs in people with type 1 diabetes whose bodies do not produce any insulin. Several things can lead to DKA, including illness, improper diet, or not taking an adequate dose of insulin. DKA can also occur in individuals with type 2 diabetes who have little or no insulin production. Ketosis is the presence of ketones. It’s not harmful. You can be in ketosis if you’re on a low-carbohydrate diet or fasting, or if you’ve consumed too much alcohol. If you have ketosis, you have a higher than usual level of ketones in your blood or urine, but not high enough to cause acidosis. Ketones are a chemical your body produces when it burns stored fat. Some people choose a low-carb diet to help with weight loss. While there is some controversy over their safety, low-carb diets are generally fine. Talk to your doctor before beginning any extreme diet plan. DKA is the leading cause of death in people under 24 years old who have diabetes. The overall death rate for ketoacidosis is 2 to 5 percent. People under the age of 30 make up 36 percent of DKA cases. Twenty-seven percent of people with DKA are between the ages of 30 and 50, 23 percent are between the ages of 51 and 70, and 14 percent are over the age of 70. Ketosis may cause bad breath. Ket Continue reading >>

Treatment Of Severe Alcohol Poisoning

Treatment Of Severe Alcohol Poisoning

Nefrologia (English Version) 2008;28:369-72 | doi: Tratamiento de las intoxicaciones graves por alcoholes a Servicio de Nefrolog??a, Hospital Universitario La Paz, Madrid, Madrid, Espa??a, b 2??rea de Tecnolog??a de la Informaci??n, SESCAM, Toledo, Toledo, Espa??a, La intoxicacin por alcoholes (metanol, etanol o etilenglicol) puede originar acidosis metablica severa con hiato aninico y/o osmolal elevados, alteraciones neurolgicas que van desde la obnubilacin al coma profundo, amaurosis, y muerte. Adems, algunos pacientes pueden desarrollar un cuadro de fracaso renal agudo [1-3]. A pesar de la terapia intensiva la morbilidad y la mortalidad de estas intoxicaciones siguen siendo muy elevadas, debido fundamentalmente al retraso en el diagnstico y en el inicio del tratamiento [4, 5]. En ausencia de una historia de ingesta de metanol, etanol o etilenglicol, el diagnstico inicial es difcil de realizar. La determinacin de los niveles sricos del alcohol txico es til, pero no siempre se encuentran disponibles inmediatamente al ingreso en el hospital. Poisoning induced by alcohols (methanol, ethanol, or ethylene glycol) may cause severe metabolic acidosis with high anion and/or osmolal gaps, neurological changes ranging from confusion to deep coma, amaurosis, and death. Some patients may also develop acute renal failure.1-3 Despite intensive treatment, morbidity and mortality of these poisonings continue to be very high, mainly because of the delay in diagnosis and start of treatment. Poisoning induced by alcohols (methanol, ethanol, or ethylene glycol) may cause severe metabolic acidosis with high anion and/or osmolal gaps, neurological changes ranging from confusion to deep coma, amaurosis, and death. Some patients may also develop acute renal failure.1-3 Despite intensive tre Continue reading >>

Postmortem Diagnosis Of Diabetes Mellitus And Its Complications

Postmortem Diagnosis Of Diabetes Mellitus And Its Complications

Diabetes mellitus has become a major cause of death worldwide and diabetic ketoacidosis is the most common cause of death in children and adolescents with type 1 diabetes. Acute complications of diabetes mellitus as causes of death may be difficult to diagnose due to missing characteristic macroscopic and microscopic findings. Biochemical analyses, including vitreous glucose, blood (or alternative specimen) beta-hydroxybutyrate, and blood glycated hemoglobin determination, may complement postmortem investigations and provide useful information for determining the cause of death even in corpses with advanced decompositional changes. In this article, we performed a review of the literature pertaining to the diagnostic performance of classical and novel biochemical parameters that may be used in the forensic casework to identify disorders in glucose metabolism. We also present a review focusing on the usefulness of traditional and alternative specimens that can be sampled and subsequently analyzed to diagnose acute complications of diabetes mellitus as causes of death. The snippet could not be located in the article text. This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the article. Postmortem diagnosis of diabetes mellitus and its complications. CURML, Centre Universitaire Romand De Medecine Legale, Lausanne University Hospital, Lausanne, Switzerland CURML, Centre Universitaire Romand De Medecine Legale Received 2015 March 2; Accepted 2015 May 11. Copyright 2015 by the Croatian Medical Journal. All rights reserved. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provid Continue reading >>

How Does Chronic Alcohol Use Affect Electrolyte Imbalance?

How Does Chronic Alcohol Use Affect Electrolyte Imbalance?

A review discusses the association between chronic alcohol use and electrolyte imbalance, and the therapies that could be adopted to address these issues. Chronic alcohol use, or alcoholism, affects roughly 4% of Canadians1 and roughly 12.5% of Americans.2 Alcohol consumption is known to increase the risk of several types of cancer, diabetes, cardiovascular disease, and liver disease in a dose-dependent manner.3Additionally, chronic alcohol use is associated with acid-base and electrolyte imbalance. A recent review published in The New England Journal of Medicine discusses these disorders, as well as the therapeutic approaches that can be adopted to treat these disorders.4 A variety of acid-base disturbances are observed in roughly 78% of the patients with chronic alcohol use. One of these is alcoholic ketoacidosis, which manifests as abdominal pain and vomiting. These symptoms are caused by gastritis and pancreatitis that follow chronic alcohol use. Clinically, alcoholic ketoacidosis is characterized by high ketone levels in the blood, a high anion gap (or an increased concentration of anions), and normal to slightly elevated glucose levels. Alcoholic ketoacidosis is a consequence of ethanol metabolism and prolonged starvation with the depletion of glycogen stores in the liver. The authors recommend that initial treatment in such patients should involve terminating the ketogenic process by intravenous administration of dextrose. Additionally, they recommend administering thiamine but not insulin or bicarbonate. Acute hypophosphatemia, or phosphorus deficiency, is seen in up to 50% of patients over the first 2-3 days after they are hospitalized for alcohol overuse. Hypophosphatemia is manifested as rhabdomyolysis (muscle breakdown) and weakness of the skeletal muscles. Continue reading >>

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis in a Patient With Isopropyl Alcohol Intoxication: A Case Report Xiaomei Meng, MD, PhD; Suman Paul, MBBS, PhD; Douglas J. Federman, MD From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Author, Article, and Disclosure Information From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterest Forms.do?msNum=L14-0336 . Background: An elevated plasma osmolal gap is common in all forms of alcohol intoxication. Methyl alcohol and ethylene glycol are metabolized to compounds that produce metabolic acidosis. Isopropyl alcohol, however, is metabolized to acetone, which does not cause metabolic acidosis and cannot be metabolized to compounds that do ( 1 ). Therefore, the presence of metabolic acidosis is used to rule out isopropyl alcohol intoxication. This distinction is important because fomepizole is used to treat methyl alcohol and ethylene glycol intoxication but is contraindicated in isopropyl alcohol intoxication because it reduces the clearance of isopropyl alcohol and thus prolongs its effects ( 2 ). Continue reading >>

Compendium

Compendium

Acute MI 2 out of 3 criteria130 minutes retrosternal pain - must R/O MI, PE, Aortic dissection2Cardiac enzymes elevated3ECG changes Unstable Angina -Chest pain at rest - cardiac ischemia w/o ECG changes MI Causes See also: Abdominal pain DdxPathophysiology Premature activation of pancreatic enzymes causing autodigestion of the pancreas. Release of lipolytic enzymes from the pancreas causes significant inflammation o Source: Academic Life in Emergency Medicine Gaze-Evoked NystagmusFrom: the patient to gaze at a target placed 20 to 30 degrees to the left and right of center for Diagnostic action Abolishes conduction through the AV node E.g. PSVT Terminates some re-entrant type tachycardiasDose 3-12 mg rapid IV push Age-appropriate Pediatric Fever Without a Source workup See also: Pediatric fever Ddx Terms:Fever without a source FWS: No adequate explanation for fever after H&P.Fever of unknown origin FUO: No adequate explanation for fever lasting at least 8 days' duration, af Sx Poor nutritionLabs Low thiamine levels due to poor nutrition Low glucose due to suppression of gluconeogenesis by alcohol (give thiamine first to prevent precipitating Wernicke's encep A BDZ, the #1 prescribed mental health drugMechanism Binds GABA-alpha receptors Enhances the affinity of GABA for the receptor, allows increased opening of the GABA-alpha channelIndications See also: COPD ExacerbationEpidemiology More common in male children than female children More common in female adults than male adults Higher prevalence in African-Americans thanTriggers Ddx Coarctation BP in arm(s) greater than legs BP in R arm greater than L arm Subclavian artery atherosclerosis & What&rsquos your name? What happened?100% O2 non-rebreather, pulse ox, cardiac monitor, BP, two Continue reading >>

Phosphate Homeostasis In Critical Care

Phosphate Homeostasis In Critical Care

Advanced Trainee in Intensive Care Medicine Consultant in Anaesthesia and Intensive Care Medicine To whom correspondence should be addressed. Tel: +44 1226 432022; E-mail: [email protected] Search for other works by this author on: BJA Education, Volume 16, Issue 9, 1 September 2016, Pages 305309, RL Wadsworth, S Siddiqui; Phosphate homeostasis in critical care, BJA Education, Volume 16, Issue 9, 1 September 2016, Pages 305309, Serum phosphate is under tight physiological control. Hypophosphataemia is common in hospitalized patients, particularly in the critically ill. Hypophosphataemia causes multisystem effects if left untreated. Phosphate disturbances are often multifactorial. Treatment of hyperphosphataemia secondary to rhabdomyolysis or tumour lysis syndrome should be instituted promptly. Phosphorus plays a critical role in many biological processes, including energy metabolism, cellular signalling, nucleic acid metabolism, membrane integrity, and bone mineralization. 1 Phosphate is an inorganic molecule containing four oxygen atoms and a central phosphorus atom. In its ionic form, phosphate is negatively charged, leading it to be an ideal buffer and easily combining with positively charged calcium ions to contribute to hydroxyapatite, the main mineral component of bone, where up to 85% of the body's phosphate stores exist. Phosphorus in the diet is present in inorganic and organic forms. Organic phosphorus is absorbed less freely than inorganic phosphate. Phosphate absorption is highly efficient, with 6070% of an intestinal load absorbed from a typical diet, 2 occurring mostly in the duodenum and jejunum. Intestinal absorption occurs both by non-regulated passive transport through the paracellular pathway and regulated active mechanisms 3 via type IIb sodium phos Continue reading >>

Emergency Medicine News

Emergency Medicine News

Thought you might appreciate this item(s) I saw at Emergency Medicine News. Your message has been successfully sent to your friend. Some error has occurred while processing your request. Please try after some time. A 44-year-old-man with a past medical history of alcohol abuse was brought to the emergency department by EMS. He was found sleeping on a bench and appeared intoxicated. His initial vital signs were temperature 90.9F, heart rate 62 bpm, blood pressure 130/84 mm Hg, respiratory rate 16 bpm, and pulse oximetry 98% on room air. He is disheveled patient, and has a depressed level of consciousness, slurred speech, and the distinct odor of mint and urine. Pertinent lab findings include an ethanol level of 340 mg/dL. The minty odor is tipoff in this case that he is inebriated from mouthwash. The ethanol concentration in mouthwashes commercially available in the United States varies widely. The highest ethanol concentration reported is 26.9 % . Alcohol-free products are also available. The risk of toxicity from the nonalcoholic ingredients is minimal in most ingestions of mouthwash: One standard drink is equivalent to 2.2 fluid ounces of 27% alcohol/volume mouthwash: National Institute on Alcohol Abuse and Alcoholism; . It is important to recognize the signs of ethanol intoxication in patients who have ingested any alcohol-containing mouthwash. Management strategies for ethanol-intoxicated patients are: n Supportive care is the mainstay of treatment. n Exclude other causes of altered mental status such as hypoglycemia, trauma, infection, co-ingestants, and stroke. n Evaluate and treat complications of ethanol intoxication such as hypothermia, hypoglycemia, and alcoholic ketoacidosis. n Nutritional support as needed: intravenous fluids with multivitamins, thiamine, a Continue reading >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev Continue reading >>

Harwood-nuss Reading For September 2016

Harwood-nuss Reading For September 2016

Spinal Trauma, Chest, Abdomen and GU Trauma: Chapters 27-35 General principles of Trauma, Trauma Airway Management, Traumatic Shock, Wound Management, Head Injuries: Chapters 18-22 Pelvic Fractures, Hip and Femur Fractures, Knee Injuries, Ankle and Foot Injuries: Chapters 42-45 Urolithiasis, Urinary Incontinence and Retention, GU stents and catheters : Chapters 126-128 Acid-Base Disturbances, Diabetes, Mellitus, Hyperglycemic Crises, Hypoglycemia, Alcoholic Ketoacidosis, Thyroid Emergencies : Chapters 203-208 Pediatrics: Diabetic Ketoacidosis and Metabolic and Endocrine Disorders : Chapter 274-275 Urinary Tract Infections in Children : Chapter 288 Hematuria, AKI, CKD/ESRD, Renal Transplant, Scrotal Pain, Penile disorders, UTI, Prostatitis, Fournier Gangrene : Chapters 117-125 Pelvic Pain, PID, Vaginal Bleeding, Vaginitis, Bartholin Gland Cyst/Abscess, Breast Masses, Sexual Assault : Chapters 129-135 Pediatrics: Hematuria and Dysuria : Chapter 243 Pediatrics: Genitourinary Disorders : Chapter 287 General Approach to Toxicology, Toxic Alcohols, Acetaminophen, Salicylates, NSAIDs, Opioids, Complications of IVDU : Chapters 295-306 Isoniazid, Organophosphates, Carbamates : Chapters 317-318 Antidysrhythmics, Local Anesthetics, Clonidine, Beta Blockers, Calcium Channel Blockers, Digoxin : Chapters 321-325 Tricyclics, Dystonia, Lithium, MAOI, SSRIs/Serotonin Syndrome, Anticholinergics, Cocaine : Chapters 339-345 PCP, Ketamine, Amphetamines : Chapter 347-348 Must be on YNHH campus or log in through Yale VPN to access links Must be on YNHH campus or log in through Yale VPN to access links Appendicitis, Bowel Obstruction, Hernias, Inflammatory Bowel Disease, Diarrhea, Diverticular Disease, Anorectal, GI Foreign Bodies, Feeding Tubes : Chapters 108-116 Bacteremia, Sepsis, and Sept Continue reading >>

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