Tricyclic Antidepressants Toxicity

Story goes like this,
A 34 yf has ingested unknown amount of TCA(Tricyclic Antidepressants) ,
The following may be true or false :

1-Pt with prominent anticholinergic toxicity  from TCA poisoning, can benefit  from physostigmine.

False

2-TCAs inhibit the fast sodium channels in the His-Purkinje system and myocardium

True

3-Most seizures are brief and self-limited

True

4-Class IA (eg, procainamide) andClass IC antiarrhythmics (eg, flecainide) can be used for refractory arrhythmias

False

5-ECG changes include R wave in AVR >3 mm; R to S ratio in AVR >0.7 &
Brugada pattern in (15%).

True

6-Consider phenytoin for ventricular dysrhythmias resistant to NaHCO3 and lidocaine and seizures resistant to benzodiazepines.

False

Recommendations:::

●Tricyclic antidepressant (TCA) usage remains common and overdose of TCA medications can be life-threatening. A summary table to facilitate the emergent management of TCA overdose is provided .

●Symptoms and signs of TCA intoxication generally consist of vital sign abnormalities, mental status changes, seizures, and anticholinergic toxicity. Sinus tachycardia and hypotension are common. Sedation is the most typical alteration in mental status, but confusion, delirium, or hallucinations may occur. Anticholinergic toxicity commonly manifests as hyperthermia, flushing, dilated pupils that respond poorly to light, delirium, intestinal ileus, and urinary retention.

●The clinical course of patients with TCA poisoning can be unpredictable, and patients who present immediately after ingestion may initially be well-appearing, only to deteriorate rapidly. Patients must be closely monitored. Maprotiline has been associated with a greater frequency of seizures and arrhythmias than other TCAs.

●Cardiac conduction abnormalities are common in patients with TCA poisoning. These abnormalities can degenerate into ventricular tachycardia and ventricular fibrillation (VT and VF), which occur in approximately 4 percent of TCA overdose cases. The electrocardiogram (ECG) is a most valuable tool in determining the extent of TCA poisoning. The following signs suggest cardiotoxicity:

•Prolongation of the QRS >100 msec

•Abnormal morphology of the QRS (eg, deep, slurred S wave in leads I and AVL)

•Abnormal size and ratio of the R and S waves in lead AVR: R wave in AVR >3 mm; R to S ratio in AVR >0.7

●Although a definitive diagnosis of TCA overdose can be made using serum measurements, such testing is typically not available to clinicians in a timely fashion and seldom plays a role in patient management. Clinically, the diagnosis of TCA poisoning is made based upon a history of ingestion, symptoms and signs consistent with the diagnosis, and characteristic ECG findings.

●Initial treatment of TCA overdose includes assessing and securing the patient’s airway, breathing, and circulation. TCA poisoned patients are frequently moribund and require intubation for airway protection and ventilation. Intravenous boluses of isotonic saline are used to treat hypotension. We recommend sodium bicarbonatetherapy for QRS duration >100 msec or any ventricular arrhythmia caused by TCA poisoning (Grade 1B). The initial dose of sodium bicarbonate is 1 to 2 mEq/kg. In adults, this may be given as two to three 50 mEq (50 mL) vials or prefilled syringes of 8.4 percent sodium bicarbonate given as a rapid IV push through a large bore IV.

●Benzodiazepines remain the treatment of choice for TCA-induced seizures. Reasonable initial treatment options in adults include diazepam 5 mg IV or lorazepam 2 mg IV. Unless bowel obstruction, ileus, or perforation is suspected, we suggest treatment with 1 g/kg of activated charcoal (maximum dose 50 g) in patients who present within two hours of ingestion (Grade 2C). Most patients respond well to standard care; for patients with refractory toxicity, management is reviewed in the text.

●Despite prominent anticholinergic toxicity in some patients, physostigmine is contraindicated as it is associated with cardiac arrest in the setting of TCA toxicity. Class IA (eg, procainamide) andClass IC antiarrhythmics (eg, flecainide) are also contraindicated.

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

Some FLASHCARDS in ED: FOAMed worth-sharing

credits: @foampodcast

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.

Paracetamol Poisoning: Learning Toxicology

A 42 YF ingested an unknown number of paracetamol tablets,
The following regarding paracetamol toxicity is/are true or false:

1-Histologic recovery lags behind clinical recovery and may take up to three months.

True, fact

2-Acute pancreatitis has been described in Stage 1.

False,
Stage 2

3-It is  suggested to treat with activated charcoal, 1 g/kg (maximum dose 50 g) by mouth for all patients who present within four hours .

True,
From Uptodate

4-Females are probably more protected than males via an increased supply and regeneration of glutathione and greater activity of conjugation enzymes .

False ,

Young children are probably protected via an increased supply and regeneration of glutathione and greater activity of conjugation enzymes 

5-Acute alcohol ingestion is not a risk factor for hepatotoxicity and may even be protective

True, fact
(From Uptodate)

Clinical manifestations of severe synthetic cannabinoid toxicity: An Update

Clinical manifestations of severe synthetic cannabinoid toxicity

Synthetic cannabinoids consist of a heterogeneous group of chemical compounds that act as agonists at cannabinoid receptors with 2 to 800 times the potency of delta-9 tetrahydrocannabinol (THC), the active component of cannabis (marijuana). They have emerged as a popular recreational drug in the United States and Europe. In an observational study of a multicenter, hospital-based registry of medical toxicology consultations, over two-thirds of 277 patients with single-agent exposure to synthetic cannabinoids had altered mental status including severe agitation, toxic psychosis, hallucinations, seizures, and coma [1]. Rhabdomyolysis and acute kidney injury were present in approximately 5 percent of these patients. There were three deaths, including a 17-year-old adolescent with sudden death after first-time inhalational use. Thus, unlike cannabis, synthetic cannabinoids have significant potential to cause serious and life-threatening toxicity among recreational users. 

Uptodate Sep 08, 2016

Commonly injured structures in Wrist: Orthopedics

Commonly injured structures in Wrist: Orthopedics

The scapholunate ligament is the most commonly injured ligament in the wrist, usually the result of a fall on an outstretched hand. The scapholunate ligament is an intrinsic ligament binding the scaphoid and lunate together between the proximal and distal rows of carpal bones. Scapholunate dissociation is diagnosed radiographically with a widening of the scapholunate space greater than 3 mm. This is also known as the Terry Thomas sign. 

Injuries to the triquetrolunate ligament are less common, and usually result from a fall onto an outstretched and dorsiflexed hand. This injury may produce pain on the ulnar aspect of the wrist and can be confused with injury to the triangular fibrocartilage complex. 

The Space of Poirier refers to the area between the two palmar arches at the junction of the capitate and lunate, and is vulnerable to ligamentous disruption.

Laceration of Tendons: Orthopedics

Laceration of Tendons

Mallet finger is the injury resulting from laceration or rupture of the extensor tendon over Zone I, the distal phalanx, or distal interphalangeal joint. This injury causes the distal interphalangeal joint to be flexed at 40 degrees. It is the most common tendon injury in athletes.

Swan neck deformity may result from chronic untreated Mallet finger. 

Boutonniere deformity results from an injury in Zone III over the proximal interphalangeal joint. Injury of the central tendon and disruption of the lateral bands allow flexion as well as the flexor digitorum profundus to function unopposed. There is retraction of the extensor hood and resultant extension of the metacarpophalangeal and distal interphalangeal joints. Gamekeeper’s thumb is the rupture of the ulnar collateral ligament. This occurs as the result of radial deviation of the metacarpophalangeal joint.

Management of tracheostomy tubes: A Minute of Meducation

Management of tracheostomy tube: 

A Minute of Meducation:

Tracheostomy tube obstruction with mucous plugging is common.

How to Manage it:

It is best treated with preoxygenation (as suctioning may cause transient hypoxia) and then placing of sterile saline into the trachea and suctioning through large flexible catheters through the inner cannula. If this does not succeed, remove the inner cannula and clean with hydrogen peroxide and rinse with water. Sometimes, the entire tracheostomy tube needs to be removed and cleaned. Tracheostomy tubes less than 7 days in maturation should be manipulated only by otolaryngology surgeons. Remember 'Pediatric' tracheostomies do not have inner cannulas.