Emergency Situations Management Flashcards
Acetaminophen overdose
1) Acetaminophen toxicity is due to centrilobular hepatic necrosis caused by N acetyl P benzoquinoneimine (napkey), which reacts with and destroys hepatocytes. Normally, this metabolite constitutes only 5% of acetaminophen metabolic products and is inactivated by conjugation with endogenous glutathione. In overdose, the supply of glutathione becomes depleted and NAPQI is not detoxified.
2) All patients who are possibly or probably at risk of hepatotoxicity and anyone for whom the time of ingestion is not known are treated with N acetylcysteine, which repletes glutathione, combines directly with N acetyl P benzoquinoneimine, and enhances sulfate conjugation of acetaminophen. Administration of N acetylcysteine is virtually 100% effective in preventing hepatotoxicity when administered within 8 hours of drug ingestion.
Airway Fire
1) Stop lasering
2) Disconnect ETT or jet catheter from patient.
3) Remove tracheal tube
4) Stop the flow of all airway gases.
5) Remove sponges and any other flammable material from airway.
6) Flood area with normal saline.
7) Use a CO2 fire extinguisher if fire persists.
8) Re-establish ventilation.
9) Ventilate with air, lower oxygen levels, if clinically appropriate.
10) Re-examine airway to see if fragments may be left behind in airway, possibly using bronchoscopy.
11) Humidified gas
12) Steroids
13) Antibiotics, ICU, and possible tracheostomy
Non-Airway OR Fire
1) Stop the flow of all airway gases.
2) Remove all drapes, flammable, and burning materials from the patient.
3) Extinguish all burning materials in, on, and around the patient, by saline, water, or smothering.
If the fire persists:
4) Use a carbon dioxide fire extinguisher in, on, or around the patient.
5) Activate the fire alarm.
6) Evacuate the patient, if feasible, following institutional protocols.
7) Close the door to the room to contain the fire and do not reopen it or attempt to reenter the room.
8) Turn off the medical gas supply to the room.
After the fire is put out:
9) Assess the patient’s status and devise a plan for ongoing care of the patient.
10) Assess for smoke inhalation injury if the patient was not intubated.
Differential Diagnosis of Amniotic Fluid Embolus:
Answer: Amniotic fluid embolus diagnosis is one of exclusion. Obstetric complications such as: 1) Post partum auto transfusion 2) Eclampsia 3) Placental abruption Non obstetrical complications such as: 4) Pulmonary embolus 5) Septic shock 6) Anaphylaxis 7) Transfusion reaction 8) Peripartum cardiomyopathy. 9) Myocardial infarction Anesthetic complications such as: 10) Local anesthetic toxicity 11) Total spinal anesthesia
Management of Amniotic Fluid Embolus:
1) Presents as respiratory failure with dyspnea, hypoxemia, hypotension and circulatory collapse.
2) 100% oxygen, intubate if necessary.
3) ACLS if necessary.
4) Large bore IVs, arterial line, central line.
5) Treat hypotension with crystalloids, blood and pressors.
6) Reduce afterload. Diuresis if needed.
7) Nitric oxide, inhaled prostacyclin if elevated pulmonary pressures from left heart failure.
8) Bloodwork: CBC, electrolytes, INR, PTT
9) Correct consumptive coagulopathy of DIC with blood products.
Anaphylaxis Initial Therapy:
1) Differential diagnosis: Asthma, light anesthesia, carcinoid, hereditary angioedema.
2) Remove trigger
3) 100 % FIO2, call for help.
4) Discontinue all anesthetic agents.
5) Start intravascular volume expansion of 2 to 4 liters of crystalloid or colloid with hypotension. For pediatrics, fluid resuscitation of 20 milliliters per kilogram of fluids.
6) Epinephrine 5 to 10 micrograms IV bolus PRN for hypotension, or 0.1 to 1 milligram IV with cardiovascular collapse.
Anaphylaxis Secondary treatment:
1) Antihistamines such as diphenhydramine 0.5 to 1 milligram per kilogram or cetirizine/ Benadryl 1 milligram per kilogram.
2) Norepinephrine or epinephrine infusion of 0.05 to 0.1 micrograms per kilogram per minute IV.
3) Bronchodilators: Salbutamol through ETT, then ketamine or magnesisum 1 to 2 milligrams if persistent.
4) Hydrocortisone 0.25 to 1 gram. Methylprednisolone 1 to 2 grams may be the drug of choice if the reaction is suspected to be mediated by complement.
5) Sodium bicarbonate of 0.5 to 1 milliequivalent per kilogram with persistent hypotension or acidosis.
6) Vasopressin for refractory shock.
7) Ranitidine 0.5 milligrams per kilogram, famotidine 20 milligrams IV, or cimetidine 300 mg IV/IM
8) Bloodwork – ABGs, tryptase between 30 minutes to 2 hours.
Angioedema:
1) Episodic subcutaneous and submucosal edema formation, often involving the face, extremities, and gastrointestinal tract.
2) One type of angioedema is caused by release of mast cell mediators and is associated with urticaria, bronchospasm, flushing, and even hypotension.
3) Treatment includes that of anaphylactic guidelines, including early administration of epinephrine (0.5 milliliters increments of 1 in 1000 IM or 0.5 milliliter boluses of 1 in 10 000 IV) is essential, or nebulized epinephrine of 2 milligrams in 3 milliliters normal saline repeated PRN.
4) The other results from bradykinin release and does not cause allergic symptoms. The most common hereditary form of angioedema results from an autosomal dominant deficiency or dysfunction of C1 esterase inhibitor. An acquired form of this deficiency may also occur through autoimmune mechanisms.
5) For the second type, the preferred treatment for an acute episode is C1 inhibitor concentrate (25 units per kilogram) or fresh frozen plasma (2 to 4 units) to replace th1e deficient enzyme.
6) Should upper airway obstruction develop during acute attacks, tracheal intubation until the edema subsides may be lifesaving.
7) When laryngoscopy is undertaken, it is important to have difficult airway equipement, personnel and equipment available to perform tracheostomy if needed, but tracheostomy itself may be extremely difficult or impossible in the face of massive airway edema.
8) Position patient in comfortably upright. Avoid medications which will decrease respiratory drive and effort. Topicalize with lidocaine spray.
9) Choose the largest ETT possible, but be prepared to use smaller sizes.
Aspirin Overdose:
1) Administration of activated charcoal.
2) Empirical administration of dextrose will help prevent low cerebrospinal fluid glucose concentrations.
3) Administration of sodium bicarbonate to increase arterial blood pH to 7.45 to 7.55 alkalinizes the urine, which dramatically increases renal clearance of salicylate.
4) Endotracheal intubation and mechanical ventilation, if undertaken, must be done very cautiously, because an abrupt decrease in salicylate-induced hyperventilation and hyperpnea may lead to life-threatening acidosis.
5) Hemodialysis is indicated for potentially lethal concentrations of salicylic acid (more than 100 milligrams per deciLiter) and for refractory acidosis, coma, seizures, volume overload, or renal failure.
Bronchospasm:
1) Presents as hypoxia, high airway pressures, wheeze, decrease bag movement.
2) Risk factors of allergy, asthma, recent URTI, light anesthesia.
3) Differential diagnosis of circuit/ ETT obstruction, mainstem intubation, laryngospasm, pulmonary edema, pneumothorax, foreign object, anaphylaxis.
4) Increase FiO2 to 100 %
5) Deepen volatile agent.
6) Salbutamol
7) Hydrocortisone 4 milligrams per kilogram IV. 1 month to a year = 25 milligrams. 1 to 6 years = 50 milligrams. 6 to 12 years = 100 milligrams. 12 to 18 years = 100 to 500 milligrams.
8) Ketamine 2 milligrams per kilogram IV
9) Magnesium sulphate of 40 milligrams per kilogram IV to max of 2 grams.
10) If unresponsive to above, give epinephrine 10 micrograms per kilogram IM or infusion of 0.02 – 0.1 microgram per kilogram per minute.
Carcinoid crisis:
1) Initial prophylactic steps to avoid release, such as anxiolytics for stress, octreotide one hundred and fifty to two hundred and fifty micrograms subQ every 6 to 8 hours.
2) Administer octreotide, a long acting somatostatin analogue.
3) Vasopressin as alternative if octreotide does not work
4) H 1, such as cetirizine or diphenhydramine and H2 blockers such as ranitidine, to block the effects of histamine.
5) Symptomatic therapy such as bronchodilators for wheezing.
6) H2 blockers, diphenhydramine and steroids to inhibit the action of bradykinin.
7) Cyproheptadine if any serotonin component.
Carbon monoxide poisoning:
1) Measurement requires a CO-oximeter, which, by spectrophotometry, can detect and quantify all normal and abnormal hemoglobins.
2) Supplemental oxygen, and aggressive supportive care: airway management, blood pressure support, and cardiovascular stabilization.
3) Oxygen therapy shortens the elimination half-time of CO by competing at the binding sites on hemoglobin and improves tissue oxygenation.
Croup:
1) Single dose dexamethasone 0.15 to 0.6 milligrams per kilogram PO or IM.
2) Or, nebulized budesonide 2 milligrams in 4 milliliters of water.
3) Severe croup should be treated with nebulized epinephrine 0.5 milliliters of 2.25% racemic epinephrine in 4.5 milliliters of normal saline. Or 0.5 milliliters of L epinephrine 1 to 1000 concentration diluted in 5 milliliters normal saline.
4) Observe patient for at least 2 to 4 hours after the last nebulized epinephrine treatment for possible return of obstructive symptoms.
5) If intubation is needed, children should be intubated with a smaller endotracheal tube that that predicted for their age.
Delirium tremens:
1) Delirium tremens occurs 2 to 4 days after the cessation of alcohol ingestion and manifests as hallucinations, combativeness, hyperthermia, tachycardia, hypertension or hypotension, and grand mal seizures.
2) Administer diazepam (5 to 10 milligrams IV every 5 minutes) or another benzodiazepine until the patient becomes sedated but remains awake.
3) Administration of β-blockers such as propranolol and esmolol is useful to suppress manifestations of sympathetic hyperactivity. The goal of β-blocker therapy is to decrease the heart rate to less than 100 beats per minute.
4) Correct fluid, electrolyte (such as magnesium, potassium), and metabolic (thiamine) derangements.
5) Lidocaine is usually effective if dysrhythmias occur despite correction of electrolyte abnormalities.
6) Protect the airway with a cuffed endotracheal tube if necessary in some patients.
Diabetes Insipidus (central):
1) Suspect if urine output is more than 100 mL/ h.
2) Order urine osmolarity (positive if less than 300 milliosmoles per liter) and serum osmolarity (positive if more than 150 milliequivalents per liter).
3) Differential diagnosis of DI includes: brain tumor, head trauma, neurosurgery, subarachnoid hemorrhage.
4) Estimate total body water deficit = 0.6 x body weight (in kilograms) x difference between patient sodium and normal sodium, which is divided by normal sodium of 140.
5) Replace water deficit over 24 to 48 hours, or 1 to 2 milliequivalents per liter per hour.
6) Hourly fluid maintenance plus two thirds of the previous hourly urine output.
7) Half normal saline and 5 percent dextrose in water are commonly used as replacement fluids due to hypo osmolar and low sodium fluid loss.
8) IV aqueous ADH of 100 to 200 milliunits per hours, with isotonic crystalloid solution.
9) If the hourly fluid requirement exceeds three hundred and fifty to four hundred milliliters, desmopressin is usually administered.
10) DDAVP subcutaneous 1 to 4 micrograms or 5 to 20 micrograms every 12 to 24 hours.
11) Measure sodium and plasma osmolality hourly until sodium is ____
Diabetic ketoacidosis:
1) Normal saline intravenous fluid of 200 – 300 milliliters per hour.
2) IV loading dose of 0.1 milligrams per kilogram of regular insulin.
3) Low dose insulin infusion of 0.1 units per kilogram per hour.
4) Measure ABGs for bicarbonate, electrolytes for potassium, and glucose hourly.
5) Replace potassium, magnesium and phosphate as needed.
6) Goal is to normalize anion gap.
7) Give D5W in normal saline when glucose is around 14.
8) Stop insulin infusion when bicarbonate is 18.
9) Then place patient on sliding scale insulin with glucose check every 4 hours.
10) Stop dextrose infusion when patient is able to eat.
HONK:
1) More fluid depletion than DKA. Need 1 to 1.5 liters per hour of hypotonic saline if osmolarity is over 320, before switching over to isotonic.
2) Glucose usually higher than DKA
3) Total potassium deficit, but increased extracellularly
Epiglottitis:
1) avoid child distress
2) Rapid transit to OR.
3) Difficult airway cart, have surgeon in the room who is adept at rigid bronchoscopy and tracheostomy in the room.
4) Induce in preferred position.
5) Inhalational induction with spontaneous ventilation. Sevo and 100% oxygen, gentle CAP to overcome obstruction.
6) IV cannulation, intubation under deep INH GA.
7) if MH susceptible - IV propofol after some Nitrous oxide inhalation
8) Fluid resuscitation, blood culture and antibiotics.
9) No muscle relaxants until intubated.
10) Potential post op ventilation for 24 - 48 hours in ICU
Foreign body:
1) Risk of airway obstruction, pneumothorax, infection if chronic.
2) NPO guidelines if stable. If hypoxic, distressed, partial obstruction will be full stomach.
3) Pre induction IV insertion.
4) Maintain spontaneous ventilation, avoid premedications.
5) Halothane, if available, is the gold standard. It is more potent and lasts longer.
6) Consider atropine 20 micrograms per kilogram for airway instrumentation with possible vagal response.
7) Lidocaine spray to avoid coughing and breath holding.
8) Discuss with surgeon whether they plan to use flexible Bronch, which they can do through ETT or LMA, or a rigid bronch, which oxygenation is through ventilation or jet vent.
9) Maintenance with inhalational agents and boluses of propofol.
10) Intubate after removal of foreign body with 0.5 size smaller ETT.
11) Give Dexamethasone, ranitidine, maxeran if full stomach. Also suction with NG if full stomach.
12) Send to ICU if significant swelling and edema, otherwise, extubate when patient is wide awake.
Gas Embolism:
1) Administer 100% oxygen which may reduce bubble size by increasing the gradient for nitrogen to move out.
2) Stop surgery, stop nitrous oxide, compress bleeding points and flood wound to prevent further air or gas entry.
3) Promptly place patient in Trendelenburg (head down) position and rotate toward the left lateral decubitus position, or place operation site below the level of the heart. This maneuver helps trap air in the apex of the ventricle, prevents its ejection into the pulmonary arterial system, and maintains right ventricular output.
4) Maintain systemic arterial pressure with fluid resuscitation and vasopressors/beta-adrenergic agents if necessary.
5) Aspirate the CVP line if present. Do not delay resuscitation to put in a line if not already present.
6) Consider transfer to a hyperbaric chamber. Potential benefits of this therapy include compression of existing air bubbles and establishment of a high diffusion gradient to speed dissolution of existing bubbles.
7) Circulatory collapse should be addressed with CPR and consideration of more invasive procedures as described above.