Erythema Multiforme

●Erythema multiforme (EM) is an acute, immune-mediated disorder that involves the skin and/ormucosal surfaces. The treatment of acute EM varies according to the severity of the acute eruption and the presence or absence of recurrent disease.

●Many cases of EM occur secondary to herpes simplex virus (HSV) infection. In patients with HSV-induced EM, treatment with oral antivirals in the acute setting does not alter the course of EM, and is not indicated.

●Most patients with EM can be managed with symptomatic therapy alone. For patients with cutaneous disease and/or mild oral mucosal involvement, treatment with topical corticosteroids, oral antihistamines, and/or an anesthetic mouthwash is sufficient.

●Severe oral mucosal involvement may be accompanied by intense pain and an inability to eat or drink. For patients with severe oral mucosal involvement, we suggest treatment with oral prednisone (40 to 60 mg/day) tapered over the course of two to four weeks (Grade 2C). Patients with disabling symptoms may require hospitalization for nutrition and pain control.

●Ocular involvement rarely may lead to keratitis, conjunctival scarring, or visual impairment. Patients with ocular symptoms should be referred to an ophthalmologist.

●Some patients with EM develop recurrent disease. When feasible, the inciting agent should be identified and eliminated. For patients with HSV-induced or idiopathic EM that recurs ≥6 times per year, or who have fewer, but disabling episodes, we recommend treatment with continuous antiviral therapy (Grade 1B).

●For patients with severe, recurrent EM who fail to respond to continuous systemic antiviral therapy, we suggest treatment with azathioprine, mycophenolate mofetil, or dapsone (Grade 2C). Other options for therapy include other immunomodulatory drugs.

NonSustained Ventricular Tachycardia

Non Sustained V Tachycardia:::

●A variety of definitions of nonsustained ventricular tachycardia (NSVT) have been published, but the most commonly used definition is three or more consecutive ventricular beats, a heart rate of >120 beats per minute, and a duration of arrhythmia of less than 30 seconds.

●Patients with NSVT are usually asymptomatic, although some patients may notice symptoms associated with episodes of NSVT. The type and intensity of symptoms, which may include palpitations, chest pain, shortness of breath, syncope, or presyncope, will vary depending upon the rate and duration of the NSVT along with the presence or absence of significant comorbid conditions.

●Few physical examination findings in patients with NSVT are unique and specific. By definition, patients will have a pulse exceeding 100 beats per minute during the episode. In addition, if the physical examination coincides with an episode of NSVT, this can reveal evidence of atrioventricular (AV) dissociation, including marked fluctuations in blood pressure, variability in the occurrence and intensity of heart sounds (especially S1), and cannon A waves.

●All patients with suspected NSVT should have a 12-lead electrocardiogram (ECG), although NSVT is frequently identified on continuous telemetric monitoring, in which case only one or two leads may be available for review.

●Once nonsustained ventricular tachycardia (NSVT) has been identified, reversible causes of arrhythmia should be sought, including electrolyte imbalances, myocardial ischemia, hypoxia, adverse drug effects, anemia, hypotension, and heart failure. For patients who have only a single asymptomatic episode of NSVT, often no further investigation is required. However, for patients with multiple episodes or for those with symptoms felt to be related to NSVT, a thorough diagnostic evaluation to exclude structural heart disease is warranted, including cardiac imaging and ambulatory ECG monitoring for most patients and invasive electrophysiology studies (EPS) only on rare occasions.

●Treatment of patients with NSVT is as follows:

•Patients with NSVT and no identified symptoms do not require any specific therapy directed toward the NSVT. However, some patients with NSVT who are found to have a cardiomyopathy with significantly reduced left ventricular systolic function may be evaluated for implantable cardioverter defibrillator (ICD) placement for primary prevention of sudden cardiac death related to sustained ventricular tachyarrhythmias.

•For the initial treatment of patients with symptomatic NSVT, we suggest beta blockers rather than calcium channel blockers or antiarrhythmic medications (Grade 2C).

•For patients with NSVT who remain symptomatic in spite of beta blockers, or who are unable to tolerate beta blockers due to side effects, we suggest adding a nondihydropyridine calcium channel blocker (ie, verapamil or diltiazem) rather than an antiarrhythmic medication

•For some patients who have frequent, highly symptomatic NSVT not adequately suppressed by beta blockers or calcium channel blockers, the addition of antiarrhythmic medications (table 1) may be helpful. We suggest amiodarone as the initial choice, rather than other antiarrhythmic drugs, based on its efficacy (Grade 2C).

•In patients who have very frequent, symptomatic monomorphic NSVT not controlled by medications or who are unable or unwilling to take medications, catheter ablation can be effective for reducing or eliminating NSVT and associated symptoms

Anion Gap and the role of Carbonic Anhydrase: Simplified

Anion Gap and the role of Carbonic Anhydrase

Carbonic anhydrase catalyses the first part of the reversible reaction in which carbon dioxide and water are converted to carbonic acid (and vice versa):
CO2 + H2O ←→ H+ + HCO3-

In the kidney, carbonic anhydrase is found in the proximal convoluted tubule.

The equation is normally shifted to the left allowing the formed carbon dioxide to diffuse back into the systemic circulation. In the presence of a carbonic anhydrase inhibitor, such as acetazolamide, the equation is shifted to the right and more H+ and HCO3- is produced. The H+ is reabsorbed alongside chloride ions. However, the bicarbonate is passed in the urine as it is not easily absorbed in the nephron. This results in a hyperchloraemic, normal anion gap metabolic acidosis.

This effect can be used therapeutically to prevent acute mountain sickness. Whereas normally the hypoxic high altitude would stimulate ventilation resulting in a respiratory alkalosis, acetazolamide use causes net renal excretion of bicarbonate, correcting this abnormality.
With respiratory alkalosis the kidneys would physiologically excrete bicarbonate, but this takes two to three days. Acetazolamide speeds this process.
The anion gap is a simple method for discerning causes of metabolic acidosis. It relies on the fact that the concentration of cations in a solution (that is, plasma) must equal the concentration of anions. Cations have positive charge, anions have negative charge.
[Cations] = [Anions]
Most ions are unmeasured and individually have a low concentration. The measured ions in sufficient concentration are sodium, potassium, chloride and bicarbonate.

Therefore:
[Na] + [K] + [unmeasured cations] = [Cl] + [HCO3] [unmeasured anions]

And rearranging:
([Na] + [K]) - ([Cl] + [HCO3]) = [unmeasured anions] - [unmeasured cations].

In health the difference between unmeasured anions and unmeasured cations, known as the anion gap, is between 10-18 mmol/l. This value is helpful in discerning causes of metabolic acidosis, as if it is raised the acidosis is due to an unmeasured ion - such as lactate, ketones, salicylate in lactic acidosis, diabetic ketoacidosis and aspirin overdose respectively.

A normal anion gap suggests an acidosis due to bicarbonate or chloride handling - such as renal tubular acidosis, diarrhoea, ammonium chloride ingestion or, in this case, acetazolamide.

Acetazolamide is a carbonic anhydrase inhibitor which may result in a metabolic acidosis. This is not the result of an increase of unmeasured anion so therefore results in a normal anion gap. Therefore it is the best answer in this case. Other causes of a metabolic acidosis with normal anion gap are renal tubular acidosis, diarrhoea, pancreatic fistula and chloric acid (such as ammonium chloride) ingestion.

A metabolic acidosis with raised anion gap occurs in the setting of an additional unmeasured anion.
This occurs in lactic acidosis, diabetic ketoacidosis, aspirin overdose and methanol or ethylene glycol poisoning.

A metabolic alkalosis may be seen in vomiting, from other diuretics or excessive bicarbonate or antacid therapy.

Respiratory acidosis is defined by a raised pCO2 and is typically related to type 2 respiratory failure. It is seen in severe COPD, asthma, pneumonia or pulmonary oedema and hypoventilation due to sedatives, muscular disease (for example, myasthenia gravis) or chest wall trauma.

Respiratory alkalosis is seen in any cause of hyperventilation, either due to anxiety, or in hypoxic states such as asthma where adequate ventilation is preserved.

Emergency Management of Agitated Patient

Emergency Management of Agitated Patient

RSI/ Airway Management Drugs

Rapid Sequence Incubation

Airway Management Drugs are listed below

Abdominal Aortic Aneurysm

Abdominal Aortic Aneurysm

Basics

Description

• Focal dilation of the aortic wall with an increase in diameter by at least 50% (>3 cm)
• 95% are infrarenal.
• Gradual expansion or rupture causes symptoms.
• Rupture can occur into the intraperitoneal or retroperitoneal spaces.
• Intraperitoneal rupture is usually immediately fatal.
• Average growth rate of 0.2 to 0.5 cm per year
• 5-year risk of rupture:
  • Aneurysms <4.0 cm: 2%
  • Aneurysms 4.0-5.0 cm: 5%
  • Aneurysms 5.0-6.0 cm: 25%
  • Aneurysms 6.0-7.0 cm: 35%
• 40-50% die before they reach the hospital.
• 50% of patients who reach the hospital alive survive.
• 5-year survival after repair is 67%.

Geriatric Considerations

• Risk increases with advanced age.
• Present in 4-8% of all patients older than 65 years
• Peak incidence:
  • Men: 5.9% at the age of 80 years
  • Women: 4.5% at the age of 90 years

Etiology

• Risk factors:
  • Male gender
  • Age >65 years old
  • Family history
  • Cigarette smoking
  • Atherosclerosis
  • Hypertension
  • Diabetes mellitus
  • Connective tissue disorders:
    • Ehlers-Danlos syndrome
    • Marfan syndrome
• Uncommon causes:
  • Blunt abdominal trauma
  • Infections of the aorta
    

Abruptio Placentae

Abruptio Placentae

Basics

Description

• Rupture of vessels in the decidua basalis leading to premature separation of the normally implanted placenta occurring after 20 weeks gestation but prior to delivery of the infant
• Incidence/prevalence:
  • Approximately 1% of all pregnancies
  • 30% of bleeding episodes in the second half of pregnancy
  • 15% of all fetal deaths
  • 6% of all maternal morality. Risk of recurrence 10–20%
• Risk factors:
  • Maternal hypertension (>140/90)
  • Trauma
  • Increased parity
  • Previous abruption
  • Tobacco use
  • Cocaine abuse
  • Preterm premature rupture of membranes, especially if associated with intrauterine infection or oligohydramnios
  • Polyhydramnios with rapid decompression on membrane rupture
  • Precipitous first twin delivery endangers second twin.
  • Fibroids or other uterine or placental abnormalities

Genetics

Inherited thrombophilias also increase the risk of abruption (factor V Leiden

Abdominal Trauma, Blunt

Abdominal Trauma, Blunt

Basics

Description

• Injury results from a sudden increase of pressure to abdomen.
• Solid organ injury usually manifests as hemorrhage.
• Hollow viscous injuries result in bleeding and peritonitis from contamination with bowel contents.

Etiology

• Sixty percent result from motor vehicle collisions.
• Solid organs are injured more frequently than hollow viscous organs.
• The spleen is the most frequently injured organ (25%), followed by the liver (15%), intestines (15%), retroperitoneal structures (13%), and kidney (12%).
• Less frequently injured are the mesentery, pancreas, diaphragm, urinary bladder, urethra, and vascular structures.

Pediatric Considerations

• Children tend to tolerate trauma better because of the more elastic nature of their tissues.
• Owing to the smaller size of the intrathoracic abdomen, the spleen and liver are more exposed to injury because they lie partially outside the bony rib cage.

Diagnosis

ABDOMINAL PAIN-causes, symptoms, management

Abdominal Pain

Description

• Parietal pain:
  • Irritating material causing peritoneal inflammation
  • Pain transmitted by somatic nerves
  • Exacerbated by changes in tension of the peritoneum
  • Pain characteristics:
    • Sharp
    • Well localized
    • Abdominal tenderness
    • Involuntary guarding
    • Rebound tenderness
    • Exacerbated by movement and coughing
• Visceral pain:
• • Distention of a viscous or organ capsule or spasm of intestinal muscularis fibers:
    • Pain is generally poorly localized.
    • Colicky with intestinal distention
    • Constant with a distended gallbladder or kidney
  • Inflammation:
    • Initially, the pain is poorly localized.
    • Focal tenderness develops as the inflammation extends to the peritoneum or localizers.
  • Ischemia from vascular disturbances:
    • Pain is severe and diffuse with catastrophic vascular emergencies
    • Pain is disproportional to the abdominal examination
• Referred pain:
  • Felt at distant location from diseased organ
  • Due to an overlapping supply by the affected neurosegment to the perceived location of pain
• Abdominal wall pain:
  • Constant
  • Aching
  • Muscle spasm
  • Involvement of other muscle groups

Etiology

• Peritoneal irritants:
  • Gastric juice
  • Fecal material
  • Pus
  • Blood
  • Bile
  • Pancreatic enzymes
• Visceral obstruction:
  • Small intestines
  • Large intestines
  • Gallbladder
  • Ureters and kidneys
  • Visceral ischemia
  • Intestinal
  • Renal
  • Splenic
• Visceral inflammation:
  • Appendicitis
  • Inflammatory bowel disorders
  • Cholecystitis
  • Hepatitis
  • Peptic ulcer disease
  • Pancreatitis
  • Pelvic inflammatory disease
  • Pyelonephritis
• Abdominal wall pain
• Referred pain:
  • The possibility of intrathoracic disease must be considered in every patient with abdominal pain.

Diagnosis

Signs and Symptoms

• General:
  • Anorexia
  • Malaise
  • Tachycardia
  • Hypotension
  • Fever
  • Nausea
  • Vomiting:
    • Etiology requiring surgical intervention is less likely when vomiting precedes the onset of pain
• Abdominal:
  • Diarrhea
  • Constipation
  • Distended abdomen
  • Abnormal bowel sounds:
    • High-pitched rushes with bowel obstruction
    • Absence of sound with ileus or peritonitis
    • Often unreliable
  • Pulsatile abdominal mass
  • Rovsing sign: