Medical Emergencies Flashcards
Most common triggers for anaphylaxis
• Foods (nuts shellfish, etc.) • Stings • Drugs (penicillin, NSAIDs, ACEI) • Radiographic contrast media • Blood products • Latex
Anaphylaxis and allergic reactions etiology
- anaphylaxis is an exaggerated immune mediated hypersensitivity reaction that leads to systemic histamine release, increased vascular permeability, and vasodilation; regardless of the etiology, the presentation and management of anaphylactic reactions are the same
- allergic (re-exposure to allergen)
- non-allergic (e.g. exercise induced)
Anaphylaxis and allergic reactions diagnostic criteria
• anaphylaxis is highly likely with any of:
- acute onset of an illness (min to hrs) with involvement of the skin, mucosal tissue and at least one of
■ respiratory compromise (e.g. dyspnea, wheeze, stridor, hypoxemia)
■ hypotension/end-organ dysfunction (e.g. hypotonia, collapse, syncope, incontinence)
2 two or more of the following after exposure to a LIKELY allergen for that patient (min to hrs)
■ involvement of the skin-mucosal tissue
■ respiratory compromise
■ hypotension or associated symptoms
■ persistent gastrointestinal symptoms (e.g. crampy abdominal pain, vomiting)
- hypotension after exposure to a KNOWN allergen for that patient (min to hrs)
■ management is also appropriate in cases which do not fulfill criteria, but who have had previous episodes of anaphylaxis
■ life-threatening differentials for anaphylaxis include asthma and septic shock
■ angioedema may mimic anaphylaxis but tends not to improve with standard anaphylaxis treatment
Anaphylaxis and allergic reactions management
• moderate reaction: generalized urticaria, angioedema, wheezing, tachycardia
■ epinephrine (1:1000) 0.3-0.5 mg (IM in lateral thigh)
■ antihistamines: diphenhydramine (Benadryl®) 25-50 mg IM
■ salbutamol (Ventolin®) 1 cc via MDI
• severe reaction/evolution: severe wheezing, laryngeal/pulmonary edema, shock
■ ABCs, may need definitive airway (e.g. ETT) due to airway edema
■ epinephrine (1:1000) 0.1-0.3 mg IV (or via ETT if no IV access) to start, repeat as needed
■ antihistamines: diphenhydramine (Benadryl®) 50 mg IV (~1 mg/kg)
■ steroids: hydrocortisone (Solucortef®) 100 mg IV (~1.5 mg/kg) or methylprednisolone (Solumedrol®) 1 mg/kg IV q6h x 24 h
■ large volumes of crystalloid may be required
Pediatric Dosing
• Epinephrine: 0.01 mg/kg IM up to 0.5mg q5-15min
• Initial crystalloid bolus: 20 mL/kg, reassess
• Epinephrine infusion: 0.1-1 µg/kg/min up to 10 µg/min
• Diphenhydramine: 1 mg/kg up to 50 mg IM/IV q4-6h
• Ranitidine: 1 mg/kg up to 50 mg PO/IV
• Methylprednisolone: 1 mg/kg up to 125 mg IV
Anaphylaxis and allergic reactions disposition
• monitor for 4-6 h in ED (minimum) and arrange follow-up with family physician in 24-48 h
• can have second phase (biphasic) reaction up to 48 h later, patient may need to be supervised
• educate patient on avoidance of allergens
• medications
■ H1 antagonist (cetirizine 10 mg PO OD or Benadryl® 50 mg PO q4-6h x3d)
■ H2 antagonist (ranitidine 150 mg PO OD x3d)
■ corticosteroid (prednisone 50 mg PO OD x5d) to prevent secondary reaction
When should anaphylaxis be suspected
Anaphylaxis should be suspected if airway, breathing, or especially circulation compromise is present after exposure to a known allergen
involvement of 2+ systems
Hypotension definition
Hypotension is defined as systolic BP >30% decrease from baseline or • Adults: <90 mmHg • ≥11 yr: <90 mmHg • 1-10 yr: <70 mmHg + 2 x age • 1 mo-1 yr: <70 mmHg
Absolute contraindications to epinephrine
Early epinephrine is lifesaving and there are no absolute contraindications
Asthma pathophysiology
chronic inflammatory airway disease with episodes of bronchospasm and inflammation resulting in reversible airflow obstruction
what is asthma silent chest and managemetn
Beware of the silent chest in asthma exacerbations. This is a medical emergency and may require emergency intubation
Asthma history and physical
- find cause(s) of asthma exacerbation (viral, environmental, etc.)
- history of asthma control; severity of exacerbations (ICU, intubation history)
- signs of respiratory distress
- vitals, specifically O2
Asthma investigations
- peak flow meter
- ± ABG if in severe respiratory distress
- CXR if diagnosis in doubt to rule out pneumonia, pneumothorax, etc.
Elements of well-controlled asthma
- Daytime symptoms <4x/wk
- Nocturnal symptoms <1x/wk
- No limitation in activity
- No absence from work/school
- Rescue inhaler use <4x/wk
- FEV1 <90% personal best
- PEF <10-15% diurnal variation
- Mild infrequent exacerbations
Asthma - respiratory arrest imminent history and physical exam and management
Exhausted, confused, diaphoretic, cyanotic Silent chest, ineffective respiratory effort Decreased HR, RR>30, pCO2>45 mmHg O2 sat <90% despite supplemental O2
100% O2, cardiac monitor, IV access Intubate (consider induction with ketamine) Short acting β-agonist (Ventolin®): nebulizer 5 mg continually Short-acting anticholinergic (Atrovent®): nebulizer 0.5 mg x 3 IV steroids: methylprednisolone 125 mg
Asthma - severe asthma history and physical exam and management
Agitated, diaphoretic, laboured respirations Speaking in words No relief from βagonist O2 sat <90%, FEV1 <50%
Anticipate need for intubation Similar to above management Magnesium sulphate 2 g IV O2 to achieve O2 sat >92%
Asthma - moderate asthma history and physical exam and management
SOB at rest, cough, congestion, chest tightness Speaking in phrases Inadequate relief from β-agonist FEV1 50-80%
O2 to achieve O2 sat >92% Short-acting β-agonist (Ventolin®): MDI or nebulizer q5min Short-acting Anticholinergic (Atrovent®): MDI or nebs x 3 Steroids: prednisone 40-60 mg PO
Asthma - mild asthma history and physical exam and management
Exertional SOB/cough with some nocturnal symptoms Difficulty finishing sentences FEV1 >80%
βagonist Monitor FEV1 Consider steroids (MDI or PO)
Asthma disposition
• discharge safe in patients with FEV1 or PEF > 60% predicted, and may be safe if FEV1 or PEF 40-60% predicted based on patient’s risk factors for recurrence of severe attack
■ risk factors for recurrence: frequent ED visits, frequent hospitalizations, recent steroid use, recent exacerbation, poor medication compliance, prolonged use of high dose β-agonists
- β-agonist MDI with aerochamber 2-4 puffs q2-4h until symptoms controlled, then prn
- initiate inhaled corticosteroids with aerochamber if not already prescribed
- if moderate to severe attack, administer prednisone 30-60 mg/d for 7 d with no taper
• counsel on medication adherence and educate on use of aerochamber
■ follow-up with primary care physician or asthma specialist
1st degree AV conduction block definition and management
prolonged PR interval (>200 msec), no treatment required
2nd degree AV block types, definition and potential complications and management
Mobitz I: gradual prolongation of PR interval then dropped QRS complex, usually benign
No management usually required
Mobitz II: PR interval constant with dropped QRS complex, can progress to 3rd degree AV block
long-term treatment for Mobitz II block – internal pacemaker
3rd degree AV block definition and management
P wave unrelated to QRS complex, PP and RR intervals constant
◆ atropine and transcutaneous pacing (atropine with caution)
◆ if transcutaneous pacing fails consider IV dopamine, epinephrine
■ long-term treatment for Mobitz II and 3rd degree block – internal pacemaker
Sinus bradycardia causes
■ can be normal (especially in athletes)
■ causes: vagal stimulation, vomiting, myocardial infarction/ischemia, increased ICP, sick sinus node, hypothyroidism, drugs (e.g. β-blockers, calcium channel blockers)
Sinus brady treatment and when to manage
■ treat if symptomatic (hypotension, chest pain)
◆ acute: atropine ± transcutaneous pacing
◆ sick sinus: transcutaneous pacing
◆ drug induced: discontinue/reduce offending drug, consider antidotes
Sinus tachy causes
■ causes: increased sympathetic tone, drugs, fever, hypotension, anemia, thyrotoxicosis, MI, PE, emotional, pain, etc.
Sinus tachy management
search for and treat underlying cause, consider β-blocker if symptomatic
Management for patient with tachydysrhythmia that is unstable
Perform immediate synchronized cardioversion
SVT with regular rhythm and not sinus tachy management
Vagal maneuvers (carotid massage, Valsalva)
adenosine 6 mg IV push, if no conversion give 12 mg, can repeat 12 mg dose once
rhythm converts: probable re-entry tachycardia (AVNRT more common than AVRT)
◆ monitor for recurrence
◆ treat recurrence with adenosine or longer acting medications
rhythm does not convert: atrial flutter, ectopic atrial tachycardia, junctional tachycardia
◆ rate control (diltiazem, β-blockers) and consult cardiology
Afib description
most common sustained dysrhythmia
no organized P waves (atrial rate >300/min)
irregularly irregular heart rate
narrow QRS (typically)
Afib etiology
C PIRATES CHF, Cardiomyopathy PE, pericarditis Ischemic heart disease Rheumatic or valvular disease Anemia Thyroid EtOH (holiday heart), elevated blood pressure Sick sinus, Stress - surgery, sepsis
Afib treatment principles and management
treatment principles:
- stroke prevention
- treat symptoms - decreases cardiac output by 20-30% (due to loss of organized atrial contractions)
- identify/treat underlying cause
acute management
■ if unstable: immediate synchronized cardioversion
■ if onset of AFib is >48 h: rate control, anticoagulate 3 wk prior to and 4 wk after cardioversion, or do transesophageal echocardiogram to rule out clot
■ if onset <48 h or already anticoagulated: may cardiovert
◆ electrical cardioversion: synchronized direct current (DC) cardioversion
◆ chemical cardioversion: procainamide, flecainide, propafenone
• long-term management rate or rhythm control, consider anticoagulation (CHADS2 score)
Management of patient with Wolff-Parkinson-White and Afib
Use amiodarone or procainamide - avoid AV nodal blocking agents (adenosine, digoxin, diltiazem, verapamil, beta blockers) as this can increase conduction through bypass tract, leading to cardiac arrest
Types of wide QRS ventricular tachydysrhythmias
Vtach
Vfib
Torsades de pointes
Vtach definition
(rate usually 140-200 bpm)
■ definition: 3 or more consecutive ventricular beats at >100 bpm
Vtach etiology
■ etiology: CAD with MI is most common cause
Vtach treatment
■ treatment: sustained VTach (>30 s) is an emergency
◆ hemodynamic compromise: synchronized DC cardioversion
◆ no hemodynamic compromise: synchronized DC cardioversion, amiodarone, procainamide
Vfib management
call a code blue
follow ACLS for pulseless arrest
Torsades de pointes description
looks like VTach but QRS ‘rotates around baseline’ with changing axis and amplitude (twisted ribbon)
Torsades de pointes etiology
prolonged QT due to drugs (e.g. quinidine, TCAs, erythromycin, quinolones), electrolyte imbalance (hypokalemia hypomagnesemia), congenital
Torsades de pointes treatment
◆ IV Mg2+, temporary overdrive pacing, isoproterenol
◆ correct cause of prolonged QT
Acute exacerbation of COPD symptoms and triggers
cardinal symptoms of AECOPD: increased dyspnea, increased coughing frequency or severity, increased sputum volume or purulence
• triggers: virus, pneumonia, urinary tract infection, PE, CHF, MI, drugs
Physical exam findings in COPD
- Wheeze
- Maximum laryngeal height ≤4 cm
- Forced expiratory time ≥6 s
- Decreased breath sounds
- Decreased cardiac dullness
What investigation is not useful in AECOPD
PFTs
What needs to be ruled out in AECOPD
Pneumothorax
CHF exacerbation
Acute MI
Pneumonia and other infectious causes
PE
AECOPD management
- oxygen: keep O2 sat 88-92% (be aware when giving O2 to chronic hypercapnic/CO2 retainers but do not withhold O2 if hypoxic)
- bronchodilators: short-acting β-agonist (salbutamol 4-8 puffs via MDI with spacer q15min x3 prn) ± short acting anticholinergic (ipratropium 4-8 puffs via MDI q15min x3 prn)
- steroids: prednisone 40-60 mg PO for 7-14 d, or methylprednisolone 125 mg IV bid-qid if severe exacerbation, or unable to take PO
- antibiotics: TMP-SMX, cephalosporins, respiratory quinolones (given if all 3 cardinal symptoms present or 2 cardinal symptoms with increased sputum purulence or mechanical ventilation)
- ventilation: apply noninvasive positive-pressure ventilation (CPAP or BiPAP) if severe distress or signs of fatigue, arterial pH <7.35, or hypercapnic
- if life-threatening, ICU admission for intubation and ventilation (chance of ventilation dependency)
AECOPE disposition
- no guidelines for admission - based on clinical judgement and comorbidities
- lower threshold to admit if comorbid illness (diabetes, CHF, CAD, alcohol abuse)
- if discharging, use antibiotics, taper steroids, up to 4-6 puffs qid of ipratropium and salbutamol and organize follow-up
Acute decompensated heart failure etiology
causes of CHF: decreased myocardial contractility (ischemia, infarction, cardiomyopathy, myocarditis)
pressure overload states (HTN, valve abnormalities, congenital heart disease)
restricted cardiac output (myocardial infiltrative disease, cardiac tamponade)
Acute decompensated heart failure precipitants
FAILURE
Forgot medication
Arrhythmia (Dysrhythmia)/Anemia
Ischemia/Infarction/Infection
Lifestyle (e.g. high salt/water intake)
Upregulation of cardiac output (pregnancy, hyperthyroidism, anemia, infection, iatrogenic fluid overload)
Renal failure
Embolism (pulmonary)
Other: hypertensive crisis, Beta blockers, CCB, NSAIDs, steroids
Acute decompensated heart failure presentation
• left-sided heart failure
■ dyspnea, SOBOE, orthopnea, PND, nocturia, fatigue, altered mental status, presyncope/syncope, angina, systemic hypotension
■ hypoxia, decreased air entry to lungs, crackles, S3 or S4, pulmonary edema (on CXR), pleural effusion (usually right-sided)
• right-sided heart failure
■ dependent bilateral pitting edema, JVP elevation and positive AJR, ascites, hepatomegaly
• patients often present with a combination of right-sided and left-sided symptoms
Acute decompensated heart failure investigation not used in emergency evaluation
echocardiogram not usually used in emergency evaluation, previous results may aid in diagnosis
Acute decompensated heart failure management
- ABCs, may require intubation if severe hypoxia
- sit upright, cardiac monitoring, and continuous pulse oximetry saline lock IV, Foley catheter (to follow effectiveness of diuresis)
• 100% O2 by mask
■ if poor response, may require BiPAP or intubation
• medical
■ diuretic (if volume overloaded): furosemide 40-80 mg IV
■ vasodilators (if sBP >100): nitroglycerin 0.3 mg SL q5min prn ± topical Nitrodur® patch (0.4-0.8 mg/h)
◆ if not responding or signs of ischemia (angina): nitroglycerine 10-20 µg/min IV, titrate to response
◆ if severe or refractory hypertension: nitroprusside 0.5 µg/kg/min, titrate to response
■ inotropes/vasopressors (if sBP <90)
◆ without signs of shock: dobutamine 2.5 µg/kg/min IV, titrate up to sBP >90 mmHg
◆ with signs of shock: dopamine 5-10 µg/kg/min IV, titrate up to sBP >90 mmHg
- treat precipitating factor - e.g. rate control (β-blocker, calcium channel blockers) or rhythm-control (electrical or chemical cardioversion) if new Afib
- cardiology or medicine consult
Acute decompensated heart failure when is hospital management required
- Acute MI
- Pulmonary edema or severe respiratory distress
- Severe complicating medical illness (e.g. pneumonia)
- Anasarca
- Symptomatic hypotension or syncope
- Refractory to outpatient therapy
- Thromboembolic complications requiring interventions
- Clinically significant dysrhythmias
- Inadequate social support for safe outpatient management
- Persistent hypoxia requiring supplemental oxygen
Acute decompensated heart failure investigations
- blood work: CBC, electrolytes, AST, ALT, bilirubin, Cr, BUN, cardiac enzymes, brain natriuretic peptide
- CXR: most useful test (see sidebar)
- ECG: look for MI, ischemia (ST elevation/depression, T-wave inversion), LVH, atrial enlargement, conduction abnormalities
• ABG: if severe or refractory to treatment
■ hypoxemia, hypercapnia, and acidosis are signs of severe CH
VTE Risk factors
Virchow’s triad: alterations in blood flow (venous s asis), injury to endothelium, hypercoagulable state (including pregnancy, use of OCP, malignancy)
THROMBOSIS Trauma, travel Hypercoagulable, HRT Recreational drugs (IVDU) Old (age >60 yr) Malignancy Birth control pill Obesity, obstetrcs Surgery, smoking Immobilization Sickness (CHF, MI, nephrotic syndrome, vasculitis)
DVT presentation
- calf pain, unilateral leg swelling/erythema/edema, palpable cord along the deep venous system on exam; can be asymptomatic
- clinical signs/symptoms are unreliable for diagnosis and exclusion of DVT; investigation often needed
DVT investigations
• use Wells’ criteria for DVT to guide investigations –>
Suspected acute DVT due to symptoms -> Complete compression u/s 1. If normal then repeat U/S in 5 days - DVT present - treat - DVT absent - no treatment
- Inconclusive or inadequate study then complete venography or MRI
- DVT present - treat
- Negative for DVT - no treatment - DVT present - treatment
• D-dimer is only useful at ruling out DVT if it’s negative in low-moderate risk patients (highly sensitive)
■ high risk of false positives in: elderly, infection, recent surgery, trauma, hemorrhage, late in pregnancy, liver disease, cancer
• U/S has high sensitivity & specificity for proximal clot but only 73% sensitivity for calf DVT (may need to repeat in 1 wk)
■ if positive – treat for DVT regardless of risk
■ if negative and low risk – rule out DVT
■ if negative and moderate to high risk – repeat U/S in 5-7 d to rule out DVT
Wells’ Criteria for DVT
Active cancer (1)
Paralysis, paresis or recent immobilization of leg (1)
Recently bedridden x 3 d or major surgery within 4 weeks (1)
Local tenderness (1)
Entire leg swollen (1)
Calf swelling 3 cm bigger than asymptomatic leg (1)
Unilateral pitting edema (1)
Collateral superficial veins (1)
Alternative Dx more likely (-2)
0: low prob
1-2: mod prob
3+: high prob
Wells’ Criteria for PE
Hemoptysis (1)
Cancer (1)
Previous hx of DVT/PE (1.5)
Recent immobility or surgery (1.5)
Tachy HR >100 (1.5)
Clinical signs of DVT (3)
Alternate Dx less likely than PE (3)
<2 low prob
2-6 intermediate prob
>6 high prob
DVT management
• LMWH unless patient also has renal failure
■ dalteparin 200 IU/kg SC q24h or enoxaparin 1.5 mg/kg SC q24h
- warfarin started at same time as LMWH (5 mg PO OD initially followed by dosing based on INR)
- LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days
• DOAC can be used in acute management of symptomatic DVT
■ rivaroxaban: 15 mg PO bid for first 21 d; 20 mg PO daily for remaining treatment (taken with food at the same time each day)
■ apixaban: 10 mg PO bid for first 7 d; 5 mg PO bid for remaining treatment
- consider thrombolysis if extensive DVT causing limb compromise
- IVC filter or surgical thrombectomy considered if anticoagulation is contraindicated
- duration of anticoagulation: 3 mo if transient coagulopathy; 6 mo if unprovoked DVT; life-long if ongoing coagulopathy
DVT management
• LMWH unless patient also has renal failure
■ dalteparin 200 IU/kg SC q24h or enoxaparin 1.5 mg/kg SC q24h
- warfarin started at same time as LMWH (5 mg PO OD initially followed by dosing based on INR)
- LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days
• DOAC can be used in acute management of symptomatic DVT
■ rivaroxaban: 15 mg PO bid for first 21 d; 20 mg PO daily for remaining treatment (taken with food at the same time each day)
■ apixaban: 10 mg PO bid for first 7 d; 5 mg PO bid for remaining treatment
- consider thrombolysis if extensive DVT causing limb compromise
- IVC filter or surgical thrombectomy considered if anticoagulation is contraindicated
- duration of anticoagulation: 3 mo if transient coagulopathy; 6 mo if unprovoked DVT; life-long if ongoing coagulopathy
PE presentation
- dyspnea, pleuritic chest pain, hemoptysis, tachypnea, cyanosis, hypoxia, fever
- clinical signs/symptoms are unreliable for diagnosis and exclusion of DVT; investigation often needed
PE investigations
• use Wells’ criteria for PE to guide investigations –>
- Determine need to investigate via PERC score
a) Positive 1+/8
Then Wells’ Criteria
1) If low then D-dimer assay
<500 ng/mL - PE excluded
>500 ng/mL - CTPA which excludes or confirms PE
2) If moderate/high then CTPA which excludes or confirms PE
b) Negative 0/8 then PE excluded
• PERC score alone can rule out PE in low risk patients (as determined by Wells’ criteria) unless patient is pregnant
• ECG and CXR are useful to rule out other causes (e.g. ACS, pneumonia, pericarditis) or to support diagnosis of PE
■ ECG changes in PE:
sinus tachycardia,
right ventricular strain (S1Q3T3),
T wave inversions in anterior and inferior leads
■ CXR findings in PE: Hampton’s hump (triangular density extending from pleura) or Westermark’s sign
• D-dimer is only useful at ruling out a PE if it is negative in low-moderate risk patients (highly sensitive)
■ if positive D-dimer or high-probability patient, then pursue CT angiography or V/Q scan
- CT angiography has high sensitivity and specificity for PE, may also suggest other etiology
- V/Q scan useful in pregnancy, when CT angiography not available, or IV contrast contraindicated
Management of PE
- treatment of PE with anticoagulation and duration of treatment is the same as for DVT
- consider thrombolysis if extensive PE causing hemodynamic compromise or cardiogenic shock
- catheter-directed thrombolysis or surgical thrombectomy rarely considered in massive PE or contraindication to anticoagulation
- often can be treated as outpatient, may require analgesia for chest pain (narcotic or NSAID)
• admit if hemodynamically unstable, require supplemental O2, major comorbidities, lack of sufficient social supports, unable to ambulate, need invasive therapy
■ referral to medicine for coagulopathy and malignancy workup
PERC score
- Age >50 yr
- HR >100 bpm
- O2 sat on RA <94%
- Prior history DVT/PE
- Recent trauma or surgery
- Hemoptysis
- Exogenous estrogen
- Clinical signs suggesting DVT
Score 1 for each question; a score 0/8 means patient has <1.6% chance having a PE and avoids further investigation. Caution using the PERC score in pregnant women as the original study excluded pregnant women
D dimer negative predictive value
> 99%
Number of patients with symptomatic proximal DVT will develop PE, often within days to weeks of the event
50%
Oral rivaroxaban for the treatment of symptomatic PE with or without DVT
A fixed-dose regimen (15 mg BID x 3 weeks followed by 20 mg PO once daily) of rivaroxaban alone was non-inferior to standard therapy (enoxaparin and warfarin) for the initial and long-term treatment of PE.
Diabetic ketoacidosis triad
hyperglycemia
ketosis
acidosis
due to severe insulin deficiency and counter regulatory hormone excess
Diabetic ketoacidosis clinical presentation
■ often young, Type 1 DM patients, (may rarely be first presentation of undiagnosed Type 2 DM) with symptoms evolving within a day
■ early signs and symptoms: polyuria, polydipsia, malaise, nocturia, weight loss
■ late signs and symptoms
◆ GI: anorexia nausea, vomiting, abdominal pain
◆ neurological: fatigue, drowsiness, stupor, coma
◆ respiratory: Kussmaul’s respiration, dyspnea (often due to acidosis), fruity ketotic breath
(D: Diuresis, dehydration, drowsy, delirium, dizziness
K: Kusmaul’s breathing ketotic breath
A: Abdominal pain, anorexia)
Diabetic ketoacidosis investigations
■ blood work: CBC, electrolytes, Ca2+, Mg2+, PO43-, Cr BUN, glucose, ketones, osmolality, AST/ALT/ ALP, amylase, troponin
■ urine: glucose and ketones
■ ABG or VBG
■ ECG (MI is possible precipitant; electrolyte disturbances may predispose to dysrhythmia)
Diabetic ketoacidosis management
■ rehydration
◆ bolus of NS, then high rate NS infusion (beware of overhydration and cerebral edema, especially in pediatric patients)
◆ beware of a pseudohyponatremia due to hyperglycemia (add 3 Na+ per 10 glucose over 5.5 mmol/L)
■ potassium
◆ essential to avoid hypokalemia: replace KCl (20 mEq/L if adequate renal function and initial K+ <5.5 mmol/L)
◆ use cardiac monitoring if potassium levels normal or low
■ insulin
◆ critical, as this is the only way to turn off gluconeogenesis/ketosis
◆ do not give insulin if K+ <3.3 mmol/L
◆ initial bolus of 5-10 U short-acting/regular insulin (or 0.2 U/kg) IV in adults (controversial – may just start with infusion)
◆ followed by continuous infusion at 5-10 U (or 0.1 U/kg) per h
◆ once the blood glucose <14 mmol/L, patient should receive their regular insulin SC injection and the infusion stopped in 1 h
◆ add D5W to IV fluids when blood glucose <15 mmol/L to prevent hypoglycemia
■ bicarbonate is not given unless patient is at risk of death or shock (typically pH <7.0)
Compare the efficacy and safety of rivaroxaban with standard therapy (enoxaparin, Vitamin K antagonist) or placebp in patients with acute symptomatic DVT, and in patients with confirmed symptomatic DVT or PE previously treated wth a Vitamin K antagonist or rivaroxaban for 6 to 12 mo
Rivaroxaban offers a single-drug approach to treatment of VTE that may improve the benefit-to-risk profile of anticoagulation.
4 criteria for DKA dx
- Hyperglycemia
- Metabolic acidosis
- Hyperketonemia
- Ketonuria
Precipitating factors in DKA
The 6 Is Infection Ischemia Infarction Intoxication Insulin missed In the family
Causes of hypoglycemia
Most common: excessive insulin use in setting of poor PO intake
Common: alcohol intoxication, sepsis, liver disease, oral anti-hyperglycemics
Rare: insulinomas, hypopituitarism, adrenal insufficiency, med side effects
Consequence of treating hyperosmolality too aggressively
cerebral edema
Hyperosmolar hyperglycemic state description
state of extreme hyperglycemia (44-133.2 mmol/L) due to relative insulin deficiency, counter-regulatory hormones excess, gluconeogenesis, and dehydration (due to osmotic diuresis)
Hyperosmolar hyperglycemic state clinical presentation
■ often older, Type 2 DM patients with more co-morbid illnesses and larger fluid losses with symptoms evolving over days to weeks, less GI symptoms and more neurological deficits than DKA including: mental disturbances, coma, delirium, seizures
■ polyuria, N/V
Hyperosmolar hyperglycemic state investigations
■ blood work: CBC, electrolytes, Ca2+, Mg2+, PO43-, Cr, BUN, glucose, ketones, osmolality
■ urine: glucose and ketones
■ ABG or VBG
■ find underlying cause: ECG, CXR, blood and urine C&S
Hyperosmolar hyperglycemic state management
■ rehydration with IV NS (total water deficit estimated at average 100 cc/kg body weight)
■ O2 and cardiac monitoring, frequent electrolyte and glucose monitoring
■ insulin is controversial
■ identify and treat precipitant if present (the 6 Is)
Hypoglycemia triad
characterized by Whipple’s triad:
low plasma glucose
symptoms suggestive of hypoglycemia
prompt resolution of symptoms with glucose
Hypoglycemia clinical presentation
■ neuroglycopenic symptoms: headaches, confusion, seizures, coma
■ autonomic symptoms: diaphoresis, nausea, hunger, tachycardia, palpitations
Hypoglycemia history and physical exam
■ last meal, known DM, prior similar episodes, drug therapy, and compliance
■ liver/renal/endocrine/neoplastic disease
■ depression, alcohol or drug use
Hypoglycemia management
■ IV access and rapid blood glucose measurement
■ D50W 50 mL IV push, glucose PO if mental status permits
■ if IV access not possible, glucagon 1-2 mg IM, repeat x 1 in 10-20 min
■ O2, cardiac, frequent blood glucose monitoring
■ thiamine 100 mg IM
■ full meal as soon as mental status permits
■ if episode due to long-acting insulin, or sulfonylureas, watch for prolonged hypoglycemia due to long t1/2 (may require admission for monitoring)
■ search for cause (most often due to exogenous insulin, alcohol, or sulfonylureas)
Hypernatremia common causes
Inadequate H2O intake (elderly/disabled) or inappropriate excretion of H2O (diuretics, Li, and DI)
Hypernatremia symptoms
Lethargy, weakness, irritability, and edema; seizures and coma occur with severe elevations of Na+ levels (>158 mmol/L)
Hypernatremia treatment
salt restrict
give free water
Hypernatremia special considerations
No more than 12 mmol/L in 24 h drop in Na+ (0.5 mmol/L/h) due to risk of cerebral edema, seizures, death
Hyponatremia common causes
Hypovolemic (GI renal, skin, blood fluid loss), euvolemc (SIADH/stress, adrenal insufficiency, hypothyroid, diet/intake), hypervolemic (CHF, cirrhosis, nephrotic syndrome
Hyponatremia symptoms
Neurologic symptoms 2º to cerebral edema, headache, decreased LOC depressed reflexes; chronic milder than acute
Hyponatremia tx
Water restrict/NPO; Seizure/Coma: 100cc 3% NaCl; Treat hypovolemia with RL and hypervolemia with furosemide
Hyponatremia special considerations
Limit total rise to 8 mmol/L in 24 h (0.5 mmol/L/h maximum) as patients are at risk of central pontine myelinolysis
Hyperkalemia common causes
Rhabdomyolysis, insulin deficiency, metabolic acidosis (e.g. acute renal failure, missed dialysis)
Hyperkalemia symptoms
Nausea, palpitations, muscle stiffness, areflexia
Hyperkalemia treatment
Protect heart: calcium gluconate Shift K+ into cells: D50W + Insulin, NaHC03, salbutamol Remove K+: Fluids+furosemide, dialysis
Hyperkalemia special considerations
High risk of dysrhythmia - ECG: peaked/narrow T wave, decreased P wave, prolonged PR interval, widening of QRS, AV block, VFib
Hypokalemia common causes
Metabolic alkalosis (e.g. diarrhea), insulin, diuretics, anorexia, salbutamol
Hypokalemia symptoms
N/V, fatigue, muscle cramps, constipation
Hypokalemia treatment
K-Dur®, K+ sparing diuretics, IV solutions with 20-40 mEq/L KCl over 3-4 h
Hypokalemia special considerations
ECG: U waves most important, flattened/inverted T waves, prolonged QT, depressed ST May need to restore Mg2+
Hypercalcemia common causes
Hyper-PTH and malignancy account for ~90% of cases
Hypercalcemia sx
Multisystem including CVS, GI (groans), renal (stones), rheumatological, MSK (bones), psychiatric (moans)
Hypercalcemia tx
Isotonic saline (+ furosemide if hypervolemic) Bisphosphonates, dialysis, chelation (EDTA or oral PO43-)
Hypercalcemia special considerations
Patients with more severe or symptomatic hypercalcemia are usually dehydrated and require saline hydration as initial therapy
Hypocalcemia common causes
Iatrogenic, low Mg2+, liver dysfunction,1º hypo-PTH
Hypocalcemia sx
Laryngospasm, hyperreflexia, paresthesia, tetany, Chvostek’s and Trousseau’s sign
Hypocalcemia tx
Acute (ionized Ca2+ <0.7 mM) requires immediate treatment: IV calcium gluconate 1-2 g in 10-20 min followed by slow infusion
Hypocalcemia special considerations
Prolonged QT interval can arise, leading to dysrhythmia as can upper airway obstruction
Hypertensive emergency (hypertensive crisis) definition
severe elevation of BP with evidence of end-organ damage (CNS, retinal, CVS, renal, GI) etiology
Hypertensive emergency (hypertensive crisis) etiology
essential HTN, emotional exertion, pain, use of sympathomimetic drugs (cocaine, amphetamine, etc.), MAOI use with ingestion of tyramine-containing food (cheese, red wine, etc.), pheochromocytoma, pregnancy
Hypertensive emergency (hypertensive crisis) signs and symptoms/complications by system
CNS - Stroke/TIA, headache, alte ed mental status, seizures, hemorrhage
Retinal -
Vision change, hemorrhage, exudates, papilledema
Renal -
Nocturia, elevated Cr, proteinuria hematuria oliguria
CVS -
Ischemia/angina, infarction, dissection (back pain), CHF
GI -
N/V, abdominal pain, elevated liver enzymes
Hypertensive emergency (hypertensive crisis) investigations
■ blood work: CBC, electrolytes, BUN, Cr ■ urinalysis ■ peripheral blood smear: to detect microangiopathic hemolytic anemia ■ CXR: if SOB or chest pain ■ ECG, troponins, CK: if chest pain ■ CT head: if neurological findings or severe headache ■ toxicology screen if sympathomimetic overdose suspected
Hypertensive emergency (hypertensive crisis) management
in general, strategy is to gradually and progressively reduce BP in 24-48 h
■ lower BP by 25% over the initial 60 min by initiating antihypertensive therapy (usually nitroprusside and labetatol)
■ if preeclampsia, immediately consult OB/GYN
■ establish arterial line; transfer to ICU for further reduction in BP under monitored setting
■ in case of ischemic stroke: do no rapidly reduce BP, maintain BP >150/100 for 5 d
■ in case of aortic dissection: rapid reduction of sBP to 110-120 STAT (do not resuscitate with IV fluids)
■ in case of excessive catecholamines: avoid β-blockers (except labetalol)
■ in case of ACS: address ischemia initially, then BP
Management of catecholamine-induced hypertensive emergencies
Avoid use of non-selective β-blockers as they inhibit β-mediated vasodilation and leave α-adrenergic vasoconstriction unopposed
What is HELLP Syndrome
HELLP Syndrome (seen only in preeclampsia/ eclampsia)
Hemolytic anemia
Elevated Liver enzymes
Low Platelet count
Hypertensive urgency definition
severely elevated BP (usually sBP >180, dBP >110) with no evidence of end-organ damage
Hypertensive urgency etiology
most commonly due to non-adherence with medications
Hypertensive urgency treatment
initiate/adjust antihypertensive therapy, monitor in ED (up to 6 h) and discharge with follow-up for 48-72 h
Acute coronary syndrome definition
new onset of chest pain, or acute worsening of previous chest pain, or chest pain at rest with:
■ negative cardiac biomarkers and no ECG changes = Unstable angina (UA)
■ positive cardiac biomarkers (elevated troponin) and no ECG changes = NSTEMI
■ positive cardiac biomarkers (elevated troponin) and ST segment elevation on ECG = STEMI
Acute coronary syndrome investigations
■ ECG STAT (as soon as ACS is suspected on history), troponin (2-6 h after symptom onset), CXR (to rule out other causes)
Acute coronary syndrome management
■ stabilize: ABCs, oxygen, IV access, cardiac monitors, oximetry
■ ASA 162-325 mg chewed and swallowed
■ nitroglycerin 0.3 mg SL q5min x 3; IV only if persistent pain, CHF, or hypertensive
◆ contraindications: hypotension, phosphodiesterase inhibitor use, right ventricular infarctions (⅓ of all inferior MIs)
■ anticoagulation: choice of anticoagulation (unfractionated heparin, LMWH, or fondaparinux) and additio al antiplatelet therapy (clopidogrel, ticagrelor, or prasugrel) depends on STEMI vs. NSTEMI and reperfusion strategy
■ early cardiology consult for reperfusion therapy
◆ UA/NSTEMI: early coronary angiography recommended if high TIMI risk score
◆ STEMI: primary percutaneous coronary intervention (within 90 min) preferred; thrombolytics if unavailable within 120 min of medical contact, symptoms <12 h and no contraindications
■ atorvastatin 80 mg to stabilize plaques
■ β-blocker if no signs of CHF, hemodynamic compromise, bradycardia, or severe reactive airway disease
■ ACEI initiated within 24 h
Sepsis and septic shock definitions
■ sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection
◆ organ dysfunction defined as a change in baseline SOFA score ≥2 points
■ septic shock: profound circulatory, cellular, and metabolic abnormalities with greater risk of mortality than with sepsis alone
◆ require vasopressors to maintain MAP ≥65 mmHg
◆ serum lactate ≥2 mmol/L without hypovolemia
Sepsis management
■ early recognition of sepsis and investigations to locate source of infection
■ identify severe sepsis with lactate or evidence of tissue hypoperfusion
■ early “goal-directed” therapy: ensure adequate organ perfusion
■ treatment priorities:
◆ ABCs, monitors, lines
◆ aggressive fluid resuscitation; consider ventilatory and inotropic support
◆ cultures, then early empiric appropriate antibiotics - consider broad spectrum and atypical coverage
◆ source control - e.g. remove infected Foley or surgery for ischemic gut
◆ monitor adequate resuscitation with vital signs, inferior vena cava on U/S, and serial lactates
Stroke and TIA definitions
stroke: sudden loss of brain function due to ischemia (80%) or hemorrhage (20%) with persistence of symptoms >24 h or neuroimaging evidence
TIA: transient episode of neurologic dysfunction from focal ischemia without acute infarction typically lasting <1 h, but defined as <24 h
Stroke and TIA clinical presentation
General - decreased LOC, changed mental status, confusion, neglect
Language/throat - Dysarthria, aphasia, swallowing difficulty
Vision - Diplopia, eye deviation, asymmetric pupils, visual field defect
Coordination - ataxia, intention tremor, lack of coordinatio
Motor -
Increased tone, loss of power, spasticity
Sensation - loss
Reflex - hyper-reflexia, clonus
patients with hemorrhagic stroke can present with sudden onset thunderclap headache that is usually described as “worst headache of life”
Stroke mimics
seizure, migraine, hypoglycemia, Todd’s paresis, peripheral nerve injury, Bell’s palsy, tumour, syncope
7 causes of emboli from the heart
- AFib
- MI
- Endocardtis
- Valvular disease
- Dilated cardiomyopathy
- Left heart myxoma
- Prosthetic valves
ACA stroke syndrome
Contralateral hemianesthesia and hemiparesis (legs > arms/face), gait apraxia, altered mental status, impaired judgement
MCA stroke syndrome
Contralateral hemianesthesia and hemiparesis (arms/face > legs), contralateral homonymous hemianopsia, ipsilateral gaze
PCA stroke syndrome
Contralateral homonymous hemianopsia, cortical blindness, impaired memory
VBA Stroke syndrome
Wide variety of cranial nerve, cerebellar, and brainstem deficits: vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, facial hypoesthesia, syncope, ataxia Loss of pain and temperature sensation in ipsilateral face and contralateral body
Differentiation of UMN VS LMN disease
Muscular deficit - muscle groups vs individual muscles
Reflexes - inc vs dec/absent
tone - inc vs dec
fasciculations - absent vs present
atrophy - absent/minimal vs present
Babinski - upgoing vs downgoing
Stroke and TIA investigations
- CBC, electrolytes, blood glucose, coagulation studies ± cardiac biomarkers ± toxicology screen
- non-contrast CT head: look for hemorrhage, ischemia
- ECG ± echocardiogram: rule out AFib, acute MI as source of emboli
- other imaging: carotid Doppler, CTA, MRA as appropriate
Stroke and TIA management
- ABCs; intubation with RSI if GCS ≤8, rapidly decreasing GCS, or inadequate airway protection reflexes
- thrombolysis: immediate assessment for eligibility; need acute onset, <4.5 h from drug administration time AND compatible physical findings AND normal CT with no bleed
- elevating head of bed if risk of elevated ICP, aspiration, or worsening cardiopulmonary status
• NPO, IV ± cardiac monitoring
■ judge fluid rate carefully to avoid overhydration (cerebral edema) as well as underhydration (underperfusion of the ischemic penumbra)
- BP control: only treat severe HTN (sBP >200, dBP >120, mean arterial BP >140) or HTN associated with hemorrhagic stroke transformation, cardiac ischemia, aortic dissection, or renal damage; use IV nitroprusside or labetalol
- glycemic control: keep fasting glucose <6.5% in acute phase (5 d)
- cerebral edema control: hyperventilation, mannitol to decrease ICP if necessary
- consult neurosurgery, neurology, medicine as indicated
Stroke and TIA medications
- acute ischemic stroke: thrombolytics (rt-PA, e.g alteplase) if within 4.5 h of symptom onset with no evidence of hemorrhage on CT scan
- antiplatelet agents: prevent recurrent stroke or stroke after TIAs, e.g. Aspirin® (1st line); clopidogrel, Aggrenox® (2nd line)
- anticoagulation: DVT prophylaxis if immobile; treat AFib if present
- follow-up for consideration of carotid endarterectomy, cardiovascular risk optimization
Candidates for thrombolysis and next steps
If patient presents within 4.5 h of onset of disabling neurological deficits greater than 60 min with no signs of resolution, they may be a candidate for thrombolysis
Do brief assessment and order stat CT head
Absolute contraindications for tPA
- Suspected subarachnoid hemorrhage
- Previous intracranial hemorrhage
- Cerebral infarct or severe HI within the past 3 mo 14
- Recent LP or arterial puncture at non-compressible site
- Brain tumour
- Metastatic cancer diagnosis
- BP >185 mmHg systolic, or >110 mmHg diastolic
- Bleeding diathesis
- Prolonged PT > 15 s or INR >1.7 Platelet count <100,000
- Blood glucose <2.8 or >22 mmol/L
- Intracranial hemorrhage on CT or large volume infarct
- Previously ADL dependent (clinical judgment)
- Seizure at onset causing postictal impairments
Relative exclusion criteria for tPA
- Only minor or rapidly improving symptoms
- Very severe symptoms (NIHSS > 22) or coma
- Major surgery within the past 14 d
- GI or urinary hemorrhage within the past 21 d
Types of dizziness
Vertigo - room spinning
lightheadedness - disconnected from environment
presyncope - almost blacking out
dysequilibrium - unstable, off-balance
Otalgia differential diagnosis
■ infections: acute otitis externa, acute otitis media, otitis media with effusion, mastoiditis, myringitis, malignant otitis externa in diabetics, herpes simplex/zoster, auricular cellulitis, external canal abscess, dental disease
■ others: trauma, temporomandibular joint dysfunction, neoplasm, foreign body, cerumen impactions, trigeminal neuralgia, granulomatosis with polyangiiti
Otalgia investigations
- C&S of ear canal discharge, if present
* CT head f suspicion of mastoiditis, malignant otitis externa
Hearing loss what do you need to rule out
rule out sudden sensorineural hearing loss (SSNHL), a medical emergency requiring high dose steroids and urgent referral
In elderly unilateral tinnitus or SNHL is what until proven otherwise
acoustic neuroma
90% of nosebleeds from where
anterior nasal septum at Kiesselbach’s plexus in Little’s area
Nosebleed etiologies
- most commonly caused by trauma (digital, blunt, foreign bodies)
- other causes: barometric changes, nasal dryness, chemicals (cocaine, Otrivin®), or systemic disease (coagulopathies, HTN, etc.)
Epistaxis investigations
- blood work: CBC, PT/PTT (as indicated)
* imaging: X-ray, CT as needed
Epistaxis treatment
- aim is to localize bleeding and achieve hemostasis
- first-aid: ABCs, clear clots by blowing nose or suctioning, lean forward, pinch cartilaginous portion of nose for 20 min twice
- assess blood loss: vitals, IV NS, cross match 2 units pRBC if significant
- if first aid measures fail twice, proceed to packing
• apply an anterior pack
■ clear nose of any clots
■ apply topical anesthesia/vasoconstrictors (lidocaine with epinephrine, cocaine, or soaked pledgets)
■ insert either a traditional Vaseline® gauze pack or a commercial nasal tampon or balloon
■ if bleeding stops, arrange follow-up in 48-72 h for reassessment and pack removal
■ if packing both nares, prophylactic anti-staphylococcal antibiotics to prevent sinusitis or toxic shock syndrome
■ if bleeding is controlled with anterior pressure, cautery with silver nitrate can be performed if the site of bleeding is identified (one side of septum only because if both are cauterized this can lead to septal perforation)
• if suspect posterior bleed or anterior packing does not provide hemostasis, consult ENT for posterior packing and further evaluation
■ posterior packing requires monitoring; can cause significant vagal response and posterior bleeding source can lead to significant blood loss, therefore usually requires admission
Epistaxis disposition
- discharge: discharged upon stabilization and appropriate follow-up; educate patients about prevention (e.g. humidifiers, saline spray, topical ointments, avoiding irritants, managing HTN)
- admission: severe cases of refractory bleeding, and most cases of posterior packing
Packing protocol for thrombocytopenic patients
use resorbable packs to avoid risk of re-bleeding caused by pulling out the removable pack
Complications of nasal packing
- Hypoxemia
- Toxic-shock syndrome
- Aspiration
- Pharyngeal fibrosis/stenosis
- Alar/septal necrosis
Vaginal bleeding etiology
• pregnant patient
■ 1st/2nd trimester pregnancy: ectopic pregnancy, abortion (threatened, incomplete, complete, missed, inevitable, septic), molar pregnancy, implantation bleeding, friable cervix (most common cause)
■ 2nd/3rd trimester pregnancy: placenta previa, placental abruption, premature rupture of membranes, preterm labour
■ other: trauma, bleeding cervical polyp, passing of mucous plug
• postpartum
■ postpartum hemorrhage, uterine inversion, retained placental tissue, endometritis
• non-pregnant patients
■ Structural (PALM- polyps, adenomyosis, leiomyoma, malignancies/hyperplasia), non-structural (COEIN - coagulopathy ovulatory, endometrial, iatrogenic, and not yet diagnosed)
Vaginal bleeding physical exam
- ABC (especially noting postural BP/HR and mucous membrane)
- abdominal examination (peritoneal signs, tenderness, distension, mass)
• speculum examination (NOT IF 2nd/3rd trimester bleeding; perform only when placenta previa is ruled out with U/S)
■ look for active bleeding, trauma/anomaly, and cervical dilatation
- bimanual examination (cervical tenderness, size of uterus, cervical length/dilatation)
- sterile gloves and speculum if pregnant
bEGA HCG level to see intrauterine changes on TVUS
Need β-hCG ≥1,200 to see intrauterine changes on transvaginal U/S
how to rule out ectopic pregnancy
An ectopic pregnancy can be ruled out by confirming an intrauterine pregnancy by bedside U/S unless the patient is using IVF due to the high risk of heterotopic pregnancy
vaginal bleeding investigations
- β-hCG test for all patients with childbearing potential
- CBC, blood and Rh type, quantitative β-hCG, PTT, INR
- type and cross if significant blood loss
- transvaginal U/S (rule out ectopic pregnancy and spontaneous abortion)
- abdominal U/S (rule out placenta previa, fetal demise, or retained products post-partum)
vaginal bleeding management
- ABCs
- pulse oximeter and cardiac monitors if unstable
- Rh immune globulin (Rhogam®) for vaginal bleeding in pregnancy and Rh-negative mother
• 1st/2nd trimester pregnancy
■ ectopic pregnancy: definitive treatment with surgery or methotrexate
■ intrauterine pregnancy, no concerns of coexistent ectopic: discharge patient with obstetrics follow-up
■ U/S indeterminate or β-hCG >1,000-2,000 IU: further workup and/or gynecology consult
■ abortions: if complete, discharge if stable; for all others, consult gynecology
• 2nd/3rd trimester pregnancy
■ placenta previa or placental abruption: obstetrics consult for possible admission
• postpartum
■ manage ABCs: start 2 large bore IV rapid infusion, type and cross 4 units of blood, consult OB/GYN immediately
• non-pregnant
■ if unstable admit to gynecology for IV hormonal therapy, possible D&C
■ non-structural abnormalities
◆ tranexamic acid (Cyklokapron®) to stabilize clots
◆ Provera® 10 mg PO OD x 10 d, warn patient of a withdrawal bleed
■ stable structural abnormalities (fibroids, polyps, endometrial thickening, adenomyosis), outpatient gynecology referral once stable
First trimester fetal complications
P egnancy failure: Spontaneous abortion
Fetal demise
Gestational trophoblastic disease
First trimester maternal complications
Ectopic pregnancy
Anemia
Hyperemesis gravidarum
UTI/pyelonephritis
2nd trimester fetal complications
Disorders of fetal growth - IUGR, Oligo/polyhydramnios
2nd trimester maternal complications
Gestational DM
Rh incompatibility
UTI/pyelonephritis
3rd trimester fetal complications
Vasa previa
3rd trimester maternal complications
Preterm labour/PPROM
Preeclampsia/eclampsia
Placenta previa
Placental abruption
Uterine rupture
DVT
Nephrolithiasis epidemiology and risk factors
10 % of population (twice as common in males)
- recurrence 50% at 5 yr
- peak incidence 30-50 yr of age
- 75% of stones <5 mm pass spontaneously within 2 wk, larger stones may require consultation
Nephrolithiasis clinical features
- urinary obstruction → upstream distention of ureter or collecting system → severe colicky pain
- may complain of pain at flank, groin, testes, or tip of penis
- writhing, N/V, hematuria (90% microscopic), diaphoresis, tachycardia tachypnea
- occasionally symptoms of trigonal irritation (frequency, urgency)
- fever, chills, rigors in secondary pyelonephritis
- peritoneal findings/anterior abdominal tenderness usually absent
Nephrolithiasis differential diagnosis of renal colic
- acute ureteric obstruction
- acute abdomen: biliary, bowel, pancreas, AAA
- urogynecological: ectopic pregnancy, torsion/rupture of ovarian cyst, testicular torsion
- pyelonephritis (fever, chills, pyuria, vomiting)
- radiculitis (L1): herpes zoster, nerve root compression
Nephrolithiasis investigations
- screening
- CBC: elevated WBC in presence of fever suggests infection
- electrolytes, Cr, BUN to assess renal function
- U/A: R&M (WBCs, RBCs, crystals), C&S
- imaging
- non-contrast spiral CT is the study of choice
- abdominal U/S may demonstrate stone or hydronephrosis (consider in females of childbearing age)
- AXR will identify large radioopaque stones (calcium, struvte, and cystine stones) but may miss smaller stones, uric acid stones, or stones overlying bony structures; consider as an initial investigation in patients who have a history of radioopaque stones and similar episodes of acute flank pain (CT necessary if film is negative)
• strain all urine for stone analysis
What urologic emergency involves stones
Obstruction + Infection = Urological Emergency Urgent urology consult
Composition of kidney stones
- 80% Calcium oxalate
- 10% Struvite
- 10% Uric acid
Nephrolithiasis management
- analgesics: NSAIDs (usually ketorolac [Toradol®], preferable over opioids), antiemetics, IV fluids
- urology consult may be indicated, especially if stone >5 mm, or if patient has signs of obstruction or infection
- α-blocker (e.g. tamsulosin) may be helpful to increase stone passage in select cases
Nephrolithiasis disposition
• most patients can be discharged • ensure patient is stable, has adequate analgesia, and able to tolerate oral medications • may advise hydration and limitation of protein, sodium, oxalate, and alcohol intake
Indications for Admission to Hospital
• Intractable pain
• Fever (suggests infection) or other evidence of pyelonephritis
• Single kidney with ureteral obstruction Bilateral obstructing stones
• Intractable vomiting
• Compromised renal function
Management of ophthalmologic foreign body
- copious irrigation with saline for any foreign body
- remove foreign body under slit lamp exam with cotton swab or sterile needle
- antibiotic drops qid until healed
- patching may not improve healing or comfort – do not patch contact lens wearers
- limit use of topical anesthetic to examination only
- consider tetanus prophylaxis
- ophthalmology consult if globe penetration suspected
Contraindications to pupil dilation
- Shallow anterior chamber
- Iris-supported lens implant
- Potential neurological abnormality requiring pupillary evaluation
- Caution with CV disease – mydriatics can cause tachycardia
Ddx red eye + light sensitivity
Iritis
Keratitis
abrasion
ulcer
Ddx unilateral red eye
Iritis
Keratitis
abrasion
ulcer
herpes simplex
acute angle closure glaucoma
Ddx significant pain + red eye
Iritis
Keratitis
abrasion
ulcer
scleritis
ddx red eye + white spot on cornea
corneal ulcer
ddx red eye + non-reactive pupil
acute glaucoma
iritis
ddx red eye + copious discharge
gonococcal conjunctivitis
ddx red eye + blurred vision
Iritis
Keratitis
abrasion
ulcer
herpes simplex
acute angle closure glaucoma
scleritis
corneal ulcer
iritis
gonococcal conjunctivitis
Acute angle closure glaucoma signs and symptoms
Unilateral red, painful eye Decreased visual acuity, halos around lights Fixed, mid-dilated pupil N/V Marked increase in IOP (>40 mmHg) Shallow anterior chamber ± cells
Acute angle closure glaucoma management
ophtho consult for laser iridotomy Topical β-blockers, adrenergics, and cholinergics Systemic carbonic anhydrase inhibitors and hyperosmotic agent
ophtho chemical burn signs and symptoms
known exposure to acids or alkali (worse) Pain, decreased visual acuity Vascularization or defects of cornea Iris and lens damage
ophtho chemical burn management
irrigate at site of accident
IV NS drip in ED with eyelid retracted Swab fornices Cycloplegic drops Topical antibiotics and patching
Orbital cellulitis signs and symptoms
Red, painful eye, decreased visual acuity Headache, fever Lid erythema edema, and difficulty opening eye Conjunctival injection and chemosis Proptosis, opthalmoplegia ± RAPD
Orbital cellulitis management
Admission, ophthalmology consult Blood cultures, orbital CT IV antibiotics (ceftriaxone+ vancomycin) Drainage of abscess
Retinal artery occlusion signs and symptoms
Sudden, painless, monocular vision loss RAPD Cherry red spot and retinal pallor on fundoscopy
Retinal artery occlusion management
Restore blood flow <2 h Massage globe Decrease IOP (topical β-blockers, inhaled O2/CO2 mix, IV Diamox®, IV mannitol, drain aqueous fluid)
Retinal detachment signs and symptoms
Flashes of light, floaters, and curtains of blackness/ peripheral vision loss Painless Loss of red reflex, decreased IOP Detached areas are grey RAPD ±
Retinal detachment management
Ophthalmology consult for scleral buckle/ pneumatic retinoplexy
Ophthalmologic emergencies
Infectious: Red eye, endophthalmitis, hypopyon, orbital cellulitis
Trauma: Globe rupture, orbital blow-out fractures, corneal injuries, eyelid laceration, hyphema, lens dislocation, retrobulbar hemorrhage, chemical burn
Painful vision loss: Acute iritis, corneal abrasion, globe rupture, lens dislocation, retrobulbar hemorrhage, optic neuritis, temporal arteritis, endophthalmitis, keratitis, acute angle closure glaucoma
Painless vision loss: Central retinal vein occlusion, amaurosis fugax, occipital stroke, retinal artery occlusion , retinal detachment
Staphylococcal scalded skin syndrome (SSSS) characteristics
◆ caused by an exotoxin from infecting strain of coagulase-positive S. aureus ◆ mostly occurs in children ◆ prodrome: fever, irritability, malaise, and skin tenderness ◆ sudden onset of diffuse erythema: skin is red, warm, and very tender ◆ flaccid bullae that are difficult to see, then desquamate in large sheets ◆ Nikolsky’s sign: gentle lateral stroking of skin causes epidermis to separate
Steven-Johnson Syndroe and Toxic Epidermal Necrolysis characteristics
◆ caused by drugs (e.g. phenytoin, sulfas, penicillins, and NSAIDs), bone marrow transplantation, and blood product transfusions ◆ usually occurs in adults ◆ diffuse erythema followed by necrosis ◆ severe mucous membrane blistering ◆ entire epidermis desquamation ◆ high mortality (>50%
Toxic shock syndrome characteristics
◆ caused by superantigen from S. aureus or GAS activating Tcell and cytokines ◆ patient often presents with onset of shock and multi organ failure, fever ◆ diffuse erythematous macular rash ◆ at least 3 organ systems involved: CNS, respiratory, GI, muscular, mucous membranes, renal, liver, hematologic, and skin (necrotizing fasciitis, gangrene)
■ vesicobullous lesions ■ Erythema Multiforme (EM) ◆ see Dermatology, D29 ◆ immunologic reaction to herpes simplex ◆ viral prodrome 1-14 d before rash ◆ “target lesion”: central grey bulla or wheal surrounded by concentric rings of erythema and normal skin
Pyoderma gangrenosum characteristics
◆ often associated with immunocompromised patients (HIV, leukemia, or lymphoma) with Gramnegative sepsis ◆ often occurs in arms, hands, feet, or perineal region ◆ usually begins as painless macule/vesicle pustule/bulla on red/blue base sloughing, leaving a gangrenous ulcer
Disseminated gonococcal infection characteristics
◆ fever, skin lesions (pustules/vesicles on erythematous base ~5 mm in diameter), arthritis (joint swelling and tenderness), and septic arthritis (in larger joints, such as knees, ankles, and elbows) ◆ most commonly in gonococcus positive women during menstruation or pregnancy ◆ skin lesions usually appear in extremities and resolve quickly (<7 d)
Meningococcemia characteristics
◆ flu-like symptoms of headache, myalgia, N/V ◆ petechial, macular, or maculopapular lesions with grey vesicular centres ◆ usually a few millimeters in size, but may become confluent and hemorrhagic ◆ usually appear in extremities, but may appear anywhere ◆ look for signs of meningeal irritation: Brudzinski, Kernig, nuchal rigidity, jolt accentuation
Dermatologic emergencies management
• general: judicious IV fluids and electrolyte control, consider vasopressors if hypotensive, prevention of infection • determine if admission and consult needed: dermatology or infectious diseases • specific management is determined by etiology
■ SSSS, TSS, DGI, and meningococcemia
◆ IV antibiotics
■ EM, SJS, and TEN
◆ stop precipitating medication
◆ fluids
◆ symptomatic treatment: antihistamines, antacids, topical corticosteroids, systemic corticosteroids (controversial), prophylactic oral acyclovir consider IVIG
◆ TEN: debride necrotic tissue, early transfer to burn centre improves outcome
Difference between SJS and TEN
SJS = <10% of BSA
SJS/TEN = 10-30% BSA
TEN = >30% BSA
Heat exhaustion definition
clinical features relate to loss of circulating volume caused by exposure to heat stress
- “water depletion”: heat exhaustion occurs if lost fluid not adequately replaced
- “salt depletion”: heat exhaustion occurs when losses replaced with hypotonic fluid
Heat stroke characteristics
• life-threatening emergency resulting from failure of normal compensatory heat shedding mechanisms • divided into classical and exertional subtypes • if patient does not respond relatively quickly to cooling treatments, consider other possible etiologies of hyperpyrexia (e.g. meningitis, thyroid storm, anticholinergic poisoning, delirium tremens, other infections)
heat exhaustion prognosis
Heat exhaustion may closely resemble heat stroke; heat exhaustion may eventually progress to heat stroke, so if diagnosis is uncertain treat as heat stroke
Heat exhaustion clinical features
Non-specific malaise, headache, fatigue
Body temp <40.5oC (usually normal)
No coma or seizures
Dehydration ( HR, orthostatic hypotension)
Heat exhaustion treatment
Rest in a cool envi onment IV NS if orthostatic hypotension; otherwise replace losses slowly PO
Classical heat stroke clinical features
Occurs in setting of high ambient temperatures (e.g. heat wave, poor ventilation) Often patients are older, poor, and sedentary or immobile Dry, hot skin Temp usually >40.5ºC Altered mental status, seizures, delirium, or coma May have elevated AST, ALT
Classical and exertional heat stroke treatment
Cool body temperature with water mist (e.g. spray bottle) and standing fans Ice water immersion also effective; monitor body temperature closely to avoid hypothermic overshoot Secure airway because of seizure and aspiration risk Give fluid resuscitation if still hypotensive after above therapy Avoid β-agonists (e.g. epinephrine), peripheral vasoconstriction, and antipyretics (e.g. ASA)
Exertional heat stroke clinical features
Occurs with high endogenous heat production (e.g. exercise) that overwhelms homeostatic mechanisms Patients often younger, more active Skin often diaphoretic Other features as for classical heat stroke, but may also have DIC, acute renal failure, rhabdomyolysis, marked lactic acidosis
Hypothermia complications
coagulopathy, acidosis, ventricular dysrhythmias (VFib), asystole, volume and electrolyte depletion
pathophysiology hyperthermia vs fever
hyperthermia is an increase in temperature by thermoregulatory failure, whereas fever is mediated by cytokine activiy
predisposing factors for hyperthermia
young persons who overexert themselves, older adults who cannot dissipate heat at rest (e.g. using anticholinergic drugs such as antihistamines or TCAs), and patients who are using anticholinergic or antiepileptic medications
Hypothermia labs
CBC, electrolytes, ABG, serum glucose, Cr/BUN, Mg2+, Ca2+, amylase, coagulation profile
Hypothermia imaging
CXR (aspiration pneumonia, pulmonary edema are common)
Hypothermia monitors
ECG, rectal thermometer, Foley catheter, NG tube, monitor metabolic status frequently
What is afterdrop phenomenon
Warming of extremities causes vasodilation and movement of cool pooled blood from extremities to core, resulting in a drop in core temperature leading to cardiac arrest
Classification of hypothermia and symptoms and signs associated
Mild
32-34.9
Tachypnea, tachycardia, ataxia, dysarthria, shivering
Moderate
28-31.9
Loss of shivering, dysrhythmias, Osborne (J) waves on ECG, dec LOC, combative behaviour, muscle rigidity, dilated pupils
Severe
<28
Coma, hypotension, acidemia, Vfib, asystole, flaccidity, apnea
Re-warming options
• gentle fluid and electrolyte replacement in all (due to cold diuresis)
• passive external re-warming
■ suitable for most stable patients with core temperature >32.2°C
■ involves covering patient with insulating blanket; body generates heat and re-warms through metabolic process, shivering
• active external re warming
■ involves use of warming blankets
■ beware of “afterdrop” phenomenon
■ safer when done in conjunction with active core re warming
• active core re-warming
■ generally for patients with core temperature <32.2°C, and/or with cardiovascular instability
■ avoids “afterdrop” seen with AER alone
■ re-warm core by using
◆ warmed humidified oxygen, IV fluids
◆ peritoneal dialysis with warm fluids
◆ gastric/colonic/pleural irrigation with warm fluids
◆ external circulation (cardiopulmonary bypass machine) is most effective and fastest
Approach to Cardiac Arrest in the Hypothermic Patient
- do all procedures gently or may precipitate VFib
- check pulse and rhythm for at least 1 min; may have profound bradycardia
- if any pulse at all (even very slow) do NOT do CPR
- if in VFib try to defibrillate up to maximum 3 shocks if core temperature <30°C
- intubate if required, ventilate with warmed, humidified O2
- medications (vasopressors, antidysrhythmics) may not be effective at low temperatures controversial; may try one dose
- focus of treatment is re-warming
fROSTBITE pathophysiolgoy
ice crystals form between cells
Frostbite classification
classified according to depth – similar to burns (1st to 3rd degree)
• 1st degree
■ symptoms: initial paresthesia, pruritus
■ signs: erythema, edema, hyperemia, no blisters
• 2nd degree
■ symptoms: numbness
■ signs: blistering (clear), erythema, edema
• 3rd degree
■ symptoms: pain, burning, throbbing (on thawing); may be painless if severe
■ signs: hemorrhagic blisters, skin necrosis, edema, no movement
• 4th degree
■ extension into subcuticular, osseous, and muscle tissues
Frostbite management
- treat for hypothermia: O2, IV fluids, maintenance of body warmth
- remove wet and constrictive clothing
- immerse in 40-42°C agitated water for 10 30 min (very painful; administer adequate analgesia)
- clean injured area and leave it open to air
- consider aspiration/debridement of blisters (controversial)
- debride skin
- tetanus prophylaxis
- consider penicillin G as frost bite injury has high risk of infection
- surgical intervention may be required to release restrictive eschars
- never allow a thawed area to re-chill/freeze
Classifying burns
• burn size
■ rule of nines; does not include 1st degree burns
• burn depth
■ superficial (1st degree): epidermis only (e.g. sunburn), painful and tender to palpation
■ superficial partial thickness (2nd degree): extends to epidermis and superficial dermis, blister formation occurs, very painful
■ deep partial thickness (2nd degree): involves hair follicles, sebaceous glands; skin is blistered, exposed dermis is white to yellow, absent sensation
■ full thickness (3rd degree): epidermis and all dermal layers; skin is pale, insensate, and charred or leathery
■ deep (4th degree): involvement of fat, muscle, even bone
burn management
- remove noxious agent/stop burning process
- establish airway if needed (indicated with burns >40% BSA or smoke inhalation injury)
- resuscitation for 2nd and 3rd degree burns (after initiation of 2 large bore IVs)
• fluid boluses if unstable
■ Parkland Formula: Ringer’s lactate 4 cc/kg/%BSA burned; give half in first 8 h, half in next 16 h; maintenance fluids are also required if patient cannot tolerate PO hydration
■ urine output is best measure of resuscitation, should be 40-50 cc/h or 0.5 cc/kg/h; avoid diuretics
- pain relief: continuous morphine infusion with breakthrough bolus
- investigations: CBC, electrolytes, U/A, CXR, ECG, ABG, carboxyhemoglobin
- burn wound care: prevent infection, clean/debride with mild soap and water, sterile dressings
- escharotomy or fasciotomy for circumferential burns (chest, extremities)
- topical antibiotics, systemic antibiotics infrequently indicated
- tetanus prophylaxis if burn is deeper than superficial dermis
how to estimate burn bsa
use palm of patient’s hand to estimate 1% of bsa affected
burn disposition
• admit
■ 2nd degree burns >10% BSA, or any significant 3rd degree burns
■ 2nd degree burns on face, hands, feet, perineum, or across major joints
■ electrical, chemical burns, and inhalation injury
■ burn victims with underlying medical problems or immunosuppressed patients
burn causes
- Thermal (flame, scald)
- Chemical
- Radiation (UV, medical/therapeutic)
- Electrical
iNHALATION injury etiology
- CO or cyanide poisoning
- direct thermal injury: limited to upper airway (above the vocal cords)
- smoke causes bronchospasm and edema from particulate matter and toxic inhalants (tissue asphyxiates, pulmonary irritants, systemic toxins)
Inhalation injury history and physical exam findings
- risk factors: closed space fires, period of unconsciousness, noxious chemicals involved
- cherry red skin (unreliable, usually post-mortem finding)
- singed nasal hairs, soot on oral/nasal membranes, sooty sputum
- hoarseness, stridor, dyspnea
- decreased LOC, confusion
- PO2 normal but O2 saturation low suggests CO poisoning
Inahalation injury investigations
- measure carboxyhemoglobin levels, co-oximetry
- ABG
- CXR ± bronchoscopy
Inhalation injuries management
- CO poisoning: 100% O2 ± hyperbaric O2 (controversial)
- direct thermal injury: humidified oxygen, early intubation, pulmonary toilet, bronchodilators, and mucolytics (N-acetylcysteine)
Bites investigations
- if bony injury or infection suspected, check for fracture and gas in tissue with x-rays
- get skull films in children with scalp bite wounds ± CT to rule out cranial perforation
- ultrasound may be helpful for identifying abscess formation as well as locating radiolucent foreign bodies in infected wounds
Bites initial management
- wound cleansing and copious irrigation as soon as possible
- irrigate/debride puncture wounds if feasible, but not if sealed or very small openings; avoid hydrodissection along tissue planes
- debridement is important in crush injuries to reduce infection and optimize cosmetic and functional repair
- culture wound if signs of infection (erythema, necrosis, or pus) obtain anaerobic cultures if wound foul smelling, necrotizing, or abscess; notify lab that sample is from bite wound
• suturing
■ vascular structures (i.e. face and scalp) are less likely to become infected, therefore consider suturing
■ allow avascular structures (i.e. pretibial regions, hands, and feet) to heal by secondary intention
■ tetanus immunization if >10 yr or incomplete primary series
Indications to consider admission for bites
- Moderate to severe infections
- Infections in immunocompromised patients
- Not responding to oral therapy
- Penetrating injuries to tendons, joints, CNS
- Open fractures
Bites prophylactic antibiotics
- types of infections resulting from bites: cellulitis, lymphangitis, abscesses, tenosynovitis osteomyelitis, septic arthritis, sepsis, endocarditis, meningitis
- a 3-5 d course of antibiotics is recommended for all bite wounds to the hand and should be considered in other bites if any high-risk factors present (efficacy not proven)
• dog and cat bites (pathogens: Pasteurella multocida, S. aureus, S. viridans)
■ 10-50% of cat bites, 5% of dog bites become infected
■ 1st line: amoxicillin + clavulanic acid
• human bites (pathogens: Eikenella corrodens, S. aureus, S. viridans, oral anaerobes)
■ 1st line: amoxi illin + clavulanic acid • rabies (see Infectious Diseases, ID20)
■ reservoirs: warm-blooded animals except rodents, lagomorphs (e.g. rabbits)
■ post-exposure vaccine is effective; treatment depends on local prevalence
Bee stings - how to diagnose, investigations and management
■ history and physical exam key to diagnosis; no lab test will confirm
■ investigations: CBC, electrolytes, BUN, Cr, glucose, ABGs, ECG
■ ABC management, epinephrine 0.1 mg IV over 5 min if shock, antihistamines, cimetidine 300 mg IV/IM/PO, steroids, β-agonists for SOB/wheezing 3 mg in 5 mL NS via nebulizer, local site management
Near drowning complications
- most common in children <4 yr and teenagers
- causes lung damage, hypoxemia, and may lead to hypoxic encephalopathy
- must also assess for shock, C-spine injuries, hypothermia, and scuba-related injuries (barotrauma, air emboli, lung re-expansion injury)
- complications: volume shifts, electrolyte abnormalities, hemolysis, rhabdomyolysis, renal, DIC
Near drowning management
- ABCs, treat for trauma, shock, hypothermia
- cardiac and O2 monitors, IV access
• intensive respiratory care
■ ventilator assistance if decreased respirations, pCO2 >50 mmHg, or pO2 <60 mmHg on maximum O2
■ may require intubation for airway protection, ventilation, pulmonary toilet
■ high flow O2/CPAP/BiPAP may be adequate but some may need mechanical ventilation with positive end-expiratory pressure
- dysrhythmias: usually respond to corrections of hypoxemia, hypothermia, and acidosis
- vomiting: very common, NG suction to avoid aspiration
- convulsions: usually respond to O2; if not, diazepam 5-10 mg IV slowly
- bronchospasm: bronchodilators
- bacterial pneumonia: prophylactic antibiotics not necessary unless contaminated water or hot tub (Pseudomonas)
- always initiate CPR in drowning-induced cardiac arrest even if patient hypothermic; continue CPR until patient is fully rewarmed
Near drowning disposition
- non-significant submersion: discharge after short observation
- significant submersion (even if asymptomatic): long period of observation (24 h) as pulmonary edema may appear late
- CNS symptoms or hypoxemia: admit
- severe hypoxemia, decreased LOC: ICU
What is secondary drowning
“Secondary drowning” where the onset of symptoms, as a result of pulmonary edema or infection, can be insidious, developing over hours, or possibly even days, must be anticipated in the near drowning patien
Approach to toxicology
A Airway (consider stabilizing the C-spine)
B Breathing
C Circulation
D1 Drugs ■ ACLS as necessary to resuscitate the patient ■ universal antidotes
D2 Draw bloods
D3 Decontamination (decrease absorption)
E Expose (look for specific toxidromes)/Examine the patient
F Full vitals, ECG monitor, Foley, X-rays
G Give specific antidotes and treatments
Reassess
Call Poison Info Centre
Obtain corroborative history
Principles of toxicology
4 principles to consder with all ingestions: • Resuscitation (ABCD3EFG) • Screening (toxidrome? clinical clues?) • Decrease absorption of drug • Inc ease elimination of drug
What are Universal antidotes
Dextrose (glucose)
• give to any patient presenting with altered LOC
• measure blood glucose prior to glucose administration if possible
• adults: 0.5-1.0 g/kg (1 2 mL/kg) IV of D50W
• children: 0.25 g/kg (2-4 mL/kg) IV of D25W
Oxygen
• do not deprive a hypoxic patient of oxygen no matter what the antecedent medical history (i.e. even COPD with CO2 retention)
• if depression of hypoxic drive, intubate and ventilate
• exception: paraquat or diquat (herbicides) inhalation or ingestion (oxygen radicals increase morbidity)
Naloxone (central µ-receptor competitive antagonist, shorter t1/2 than naltrexone)
• antidote for opioids: administration is both diagnostic and therapeutic (1 min onset of action)
• used for the undifferentiated comatose patient
• loading dose ■ adults ◆ response to naloxone can be drastic, so stepwise delivery of initial 2 mg bolus is recommended ◆ draw up 2 mg to deliver IV/IM/SL/SC or via ETT (ETT dose = 2 25x IV dose) – 1st dose 0.4 mg – if no response, deliver second dose 0.6 mg – if still no response, deliver remaining 1 mg ■ child ◆ 0.01 mg/kg initial bolus IV/IO/ETT ◆ 01 mg/kg if no response and opioid still suspected to max of 10 mg ■ maintenance dose ◆ may be required because half-life of naloxone (30-80 min) is much shorter than many opioids ◆ hourly infusion rate at 2/3 of initial dose that allowed patient to be roused
Thiamine (Vitamin B1) • 100 mg IV/IM with IV/PO glucose to all patients • given to prevent/treat Wernicke’s encephalopathy • a necessary cofactor for glucose metabolism (may worsen Wernicke’s encephalopathy if glucose given before thiamine), but do not delay glucose if thiamine unavailable • must assume all undifferentiated comatose patients are at risk
When is thiamine deficient
hiamine is deficient in the malnourished. Consider in patients with alcohol use disorder, anorexia, or malnutrition states
Potential adverse effect of nalaxone administration
Administration of naloxone can cause opioid withdrawal in chronic users:
Minor withdrawal may present as lacrimation, rhinorrhea, diaphoresis, yawning, piloerection, HTN, and tachycardia
Severe withdrawal may present as hot and cold flashes, arthralgias, myalgias, N/V, and abdominal cramps
Investigations for toxicology
• essential tests
■ CBC, electrolytes, BUN/Cr, glucose, INR/PTT, osmolality
■ ABGs, measure O2 sat
■ ASA, acetaminophen, EtOH levels
• potentially useful tests
■ drug levels – this is NOT a serum drug screen
■ Ca2+, Mg2+, PO43–
■ protein, albumin, lactate, ketones, liver enzymes, CK – depending on drug and clinical presentation
Serum Drug Levels
• treat the patient, not the drug level
• negative toxicology screen does not rule out a toxic ingestion – signifies only that the specific drugs tested were not detectable in the specimen
• specific drugs available on general screen vary by institution; check before ordering
• urine screens also available (qualitative only)
Urine drug screen is costly and generally not helpful in the ED management of the poisoned patient
Metabolic acidosis with increased anion gap differential diagnosis
“MUDPILES CAT” (* = toxic)
Methanol*
Uremia
Diabetic ketoacidosis/Starvation ketoacidosis
Phenformin/Paraldehyde
Isoniazid, Iron, Ibuprofen
Lactate (anything that causes seizures or shock)
Ethylene glycol*
Salicylates*
Cyanide, CO*
Alcoholic ketoacidosis
Toluene, theophylline*
Metabolic acidosis with increased plasma osmolar gap differential diagnosis
“MAE DIE” (if it ends in “-ol”, it will likely increase the POG)
Methanol Acetone Ethanol Diuretics (glycerol, mannitol, sorbitol) Isopropanol Ethylene glycol
Note: normal POG does not rule out toxic alcohol; only an elevated gap is helpful
Metabolic acidosis with decreased anion gap differential diagnosis
Electrolyte imbalance (increased Na+/K+/Mg2+)
Hypoalbuminemia (50% fall in albumin ~5.5 mmol/L decrease in the AG)
Lithium, br mine elevation
Paraproteins (multiple myeloma)
Increased O2 saturation gap ddx
Carboxyhemoglobin
Methemoglobin
Sulfmethemoglobin
Normal anion gap ddx
High K+: pyelonephritis, obstructive nephropathy, renal tubular acidosis IV, TPN
Low K+: small bowel losses, acetazolamide, renal tubular acidosis I, II
How to calculate anion gap
Na - Cl - HCO3
normal AG 0-12 mM/L
Hypoventilation or hyperventilation (pCO2) selected poisoning causes
CNS depressants (opioids, sedative-hypnotic agents, phenothiazines, EtOH)
Salicylates
CO
other asphyxiants
AG metabolic acidosis, hyperkalemia, hypokalemia selected poisoning causes
“MUDPILES CAT”
Digitalis glycosides, fluoride, potassium Theophylline, caffeine, β-adrenergic agents, soluble barium salts, diuretics, insulin
Hypoglycemia selected poisoning causes
Oral hypoglycemic agents, insulin, EtOH, ASA
Elevated osmolar gap selected poisoning causes
MAE DIE
Wide QRS complex, prolonged QT interval, AV block selected poisoning causes
TCAs, quinidine, other class Ia and Ic antidysrhythmic agents Terfenadine, astemizole, antipsychotics Ca2+ antagonists, digitalis glycosides, phenylpropanolamin
Radioopaque pills or objects on AXR ddx
“CHIPES”: Calcium, Chloral hydrate, CCl4 Heavy metals, Iron, Potassium, Enteric coated Salicylates, and some foreign bodies
Serum acetaminophen Elevated level (>140 mg/L or 1,000 µmol/L 4 h after ingestion) ddx
may be only sign of acetaminophen poisoning
Ocular decontamination
saline irrigation to neutralize pH; alkali exposure requires ophthalmology consult
Dermal decontamination (wear protective gear)
remove clothing, brush off toxic agents, irrigate all external surfaces
GI decontamination
• single dose activated charcoal
■ adsorption of drug/toxin to activated charcoal prevents availability
■ contraindications: caustics, small bowel obstruction, perforation
■ dose: 10 g/g drug ingested or 1g/kg body weight
■ odourless, tasteless, prepared as slurry with H2O
• whole bowel irrigation
■ 500 mL/h (child) to 2,000 mL/h (adult) of polyethylene glycol solution by mouth until clear effluent per rectum
■ start slow (500 mL in an adult) and aim to increase rate hourly as tolerated
■ indications
◆ awake, alert, can be nursed upright OR intubated and airway protected
◆ delayed release product
◆ drug/toxin not bound to charcoal
◆ drug packages (if any evidence of breakage emergency surgery)
◆ recent toxin ingestion
• contraindications
■ evidence of ileus, perforation, or obstruction
• surgical removal in extreme cases
■ indicated for drugs that are toxic, form concretions, or cannot be removed by conventional means
• no evidence for the routine use of cathrtics (i.e. ipecac)
Urine alkalinization indication and purpose and procedure
- may be used for: ASA, methotrexate, phenobarbital, chlorpropamide
- weakly acidic substances can be trapped in alkali urine (pH >7.5) to increase elimination
fluid resuscitate first, then 3 amps NaHCO3/L of D5W at 1.5x maintenance
• add 20-40 mEq/L KCl if patient is able to urinate
Multidose activated charcoal indications, purpose and regimens
• may be used for: carbamazepine, phenobarbital, quinine, theophylline • for toxins which undergo enterohepatic recirculation • removes drug that has already been absorbed by drawing it back into GI tract • various regimens: 12.5 g (1/4 bottle) PO q1h or 25 g (1/2 bottle) PO q2h until non-toxic
Hemodialysis indications for toxins
■ toxins that have high water solubility, low protein binding, low molecular weight, adequate concentration gradient, small volume of distribution, or rapid plasma equilibration
■ removal of toxin will lead to clinical improvement
■ advantage is shown over other modes of therapy
■ predicted that drug or metabolite will have toxic effects
■ impairment of normal routes of elimination (cardiac, renal, or hepatic)
■ clinical deterioration despite maximal medical support
Hemodialysis is usedful for what toxins
- methanol • ethylene glycol • salicylates
- lithium • phenobarbital • chloral hydrate ( trichloroethanol) • others include theophylline, carbamazepine, valproate, methotrexate
Anticholinergix toxidrome signs and symptoms
Hyperthermia
Dilated pupils
Dry skin
Vasodilation
Agitation/hallucinations
Ileus
Urinary retention
Tachycardia
“Hot as a hare” “Blind as a bat” “Dry as a bone” “Red as a beet” “Mad as a hatter” “The bowel and bladder lose their tone and the heart goes on alone”
Anticholinergix toxidrome examples of drugs
Antidepressants (TCAs)
Cyclobenzaprine (Flexeril®) Carbamazepine Antihistamines (e.g. diphenhydramine) Antiparkinsonians Antipsychotics Antispasmodics Belladonna alkaloids (e.g. atropine)
Cholinergis toxidrome signs and symptoms
“DUMBELS” Diaphoresis, Diarrhea, Decreased BP
Urination
Miosis
Bronchospasm, Bronchorrhea, Bradycardia
Emesis, Excitation of skeletal muscle
Lacrimation
Salivation, Seizures
Cholinergic examples of drugs
Natural plants: mushrooms, trumpet flower
Anticholinesterases physostigmine Insecticides (organophosphates, carbamates) Nerve gases
Extrapyramidal toxidrome signs and symptoms
Dysphonia, dysphagia Rigidity and tremor Motor restlessness, crawling sensation (akahisia) Constant movements (dyskinesia) Dystonia (muscle spasms, laryngospasm trismus, oculogyric crisis, torticollis
Extrapyramidal examples of drugs
Major tranquilizers
Antipsychotics
Hemoglobin derangement signs and symptoms
Increased respiratory rate Decreased LOC Seizures Cyanosis unresponsive to O2 Lactic acidosis
Hemoglobin derangement examples of drugs
CO poisoning (carboxyhemoglobin) Drug ingestion (methemoglobin, sulfmethemoglobin
Opioid, sedative/hypnotic, EtOH signs and symptoms
Hypothermia Hypotension Respiratory depression Dilated or constricted pupils (pinpoint in opioid) CNS depression
Sympathomimetic toxidrome signs and symptoms
Increased temperature CNS excitation (including seizures) Tachycardia, HTN N/V Diaphoresis Dilated pupils
Sympathomimetic toxidrome drugs
Amphetamines, caffeine, cocaine, LSD, phencyclidine Ephedrine and other decongestants Thyroid hormone Sedative or EtOH withdrawal
Serotonin syndrome toxidrome signs and symptoms
Mental status changes, autonomic hyperactivity, neuromuscular abnormalities, hyperthermia, diarrhea, HTN
Serotonin syndrome drugs
MAOI, TCA, SSRI, opiate analgesics Cough medicine, weight reduction medications
Protocol for Warfarin Overdose
Management: Consider Prothrombin Complex Concentrate (Octaplex®, Beriplex®) for any elevated INR, AND either life-threatening bleeding, or a plan for the patient to undergo a surgical procedure within the next 6 h
INR <5 Cessation of warfarin administration, observation, serial INR/PT
INR 5.1-9
If no risk factors for bleeding, hold warfarin x 1-2 d and reduce maintenance dose OR Vitamin K 1-2 mg PO if patient at increased risk of bleeding
INR 9.1-20
Hold warfarin, vitamin K 2-4 mg PO, serial INR/PT, additional vitamin K if necessary
INR >20
Hold warfarin, vitamin K 10 mg IV over 10 min, increase vitamin K dosing (q4h) if needed
Acetaminophen toxicity management
Decontaminate (activated charcoal)
N-acetylcysteine
Often clinically silent; evidence of liver/renal damag delayed >24 h
Toxic dose >200 mg/kg (>7.5 g adult)
Monitor drug level 4 h post-ingestion; also lver enzymes, INR, PTT, BUN, Cr
Hypoglycemia, metabolic acidosis, encephalopathy poor prognosis
Acute dystonic reaction management
Benztropine: 1-2 mg IM/IV then 2 mg PO x 3 d OR Diphenhydramine 1-2 mg/kg IV then 25 mg PO qid x 3 d
Anticholinergic toxicity management
Decontaminate (activated charcoal)
supportive care
special antidotes available; consult poison information centre
ASA toxicity management
Decontaminate (activated charcoal) Alkalinize urine; want urine pH >7.5
Monitor serum pH and drug levels closely
Monitor K+ level; may require supplement for urine alkalinization
Hemodialysis may be needed if intractable metabolic acidosis, very high levels, or end-organ damage (i.e. unable to diurese)
Benzodiaepine tox management
Decontaminate (activated charcoal)
Flumazenil
Supportive care
Beta blocker tox management
Decontaminate (activated charcoal)
Consider high dose insulin euglycemia therapy
Some dialyzable, some use intralipids
Consult poison info centre
CCB tox treatment
Decontaminate (activated charcoal)
CaCl2 1-4 g of 10% solution IV if hypotensive
Other: high dose insulin euglycemia inotropes or intralipids
Order ECG, electrolytes (especially Ca2+, Mg2+, Na+, K)
Cocaine tox management
Decontaminate (activated charcoal) if oral
Aggressive supportive care
Intralipid for life-threatening symptoms
What is contraindicated in acute cocaine toxicity
Beta blockers
CO poisoning management
supportive care
100% O2
Cyanide tox management
hydroxocobalamin
dig tox management
Decontaminate (activated charcoal)
Digoxin-specific Ab fragments 10-20 vials IV if acute; 3-6 if chronic 1 vial (40 mg) neutralizes 0.5 mg of toxin
Use for life-threatening dysrhythmias unresponsive to conventional therapy, 6 h serum digoxin >12 nmol/L, initial K+ >5 mmol/L, ingestion >10 mg (adult)/>4 mg (child)
Common dysrhythmias with dig tox
Common dysrhythmias include VFib, VTach, and conduction blocks
Ethanol tox managment
Thiamine 100 mg IM/IV
Manage airway and circulatory support
Hypoglycemia very common in children
Mouthwash = 70% EtOH; perfumes and colognes = 40-60% EtOH
Order serum EtOH level and glucose level; treat glucose level appropriately
Ethylene glycol/methanol tox management
Fomepizole (4-methylpyrazole) 15 mg/kg IV load over 30 min, then 10 mg/kg q12h OR Ethanol (10%) 10 mL/kg over 30 min, then 1.5 mL/h
CBC, electrolytes, glucose, ethanol level Consider hemodialysis
Heparin tox management
Protamine sulfate 25-50 mg IV
For unfractionated heparin od only
Insulin IM/SC/oral tox/ hypoglycemic management
Glucose IV/PO/NG
Glucagon 1-2 mg IM if no access to glucose
Consider octreotide for oral hypoglycemics (50-100 µg SC q6h); consult local Poison Information Centre
What carries highest risk of hypoglycemia among oral agents
Glyburide
MDMA tox management
decontaminate (activated charcoal)
supportive care
monitor CK - treat rhabdo with high flow fluids and aggressive external cooling for hyperthermia
TCA tox managmeent
Decontaminate (activated charcoal)
Aggressive supportive care
NaHC03 bolus for wide QRS/seizures
Also consider cardiac and hypotension support, seizure control Intralipid therapy (consult local Poison Information Centre)
What is contraindicated in combined TCA and benzo overdose
Flumazenil antidote
Acute alcohol intoxication presentation
slurred speech, CNS depression, disinhibition, lack of coordination
- nystagmus, diplopia, dysarthria, ataxia may progress to coma
- hypotension (peripheral vasodilation)
Acute alcohol intoxication obtunded ddx
head trauma/intracranial hemorrhage
■ associated depressants/street drugs, toxic alcohols
◆ may also contribute to respiratory/cardiac depression
■ hypoglycemia (screen with bedside glucometer)
■ hepatic encephalopathy: confusion, altered LOC, coma
◆ precipitating factors: GI bleed, infection, sedation, electrolyte abnormalities, protein meal
■ Wernicke’s encephalopathy (ataxia, ophthalmoplegia, delirium)
■ post-ictal state, basilar stroke
Alcohol intoxication and informed consent
Alcohol intoxication may invalidate informed consent
Alcohol intoxication and level correlation
Alcohol levels correlate poorly with intoxication
Alcohol withdrawal treatment
■ diazepam 10-20 mg IV/PO or lorazepam 2-4 mg IV/PO q1h until calm
◆ frequency of dosing may have to be increased depending on clinical response
■ may use CIWA protocol and give benzodiazepines as above until CIWA <10
■ thiamine 100 mg IM/IV then 50-100 mg/d
■ magnesium sulfate 4 g IV over 1-2 h (if hypomagnesemic)
■ admit patients with DT or multiple seizures
Common deficiencies associated with alcohol
- Thiamine
- Niacin
- Folate
- Glycogen
- Magnesium
- Potassium
Calcium
Phosphate
Alcohol withdrawal signs and progression
Time since last drink 6-8 h - mild withdrawal
Generalized tremor, anxiety, agitation, but no delirium Autonomic hyperactivity (sinus tachycardia), insomnia, N/V
1-2 d since last drink - alcoholic hallucinations
Visual (most common), auditory, and tactile hallucinations Vitals often normal
8h-2d since last drink - Withdrawal seizures
Typically brief generalized tonic-clonic seizures May have several within a few hours CT head if focal seizures have occurred
3-5 d since last drinks - DT
5% of untreated withdrawal patients Severely confused state, fluctuating LOC Agitation, insomnia, hallucinations/delusions, tremor Tachycardia, hyperpyrexia, diaphoresis High mortality rate
Cardiovascular complications of etoh withdrawal
- HTN
- cardiomyopathy: SOB, edema
- dysrhythmias (“holiday heart”)
- AFib (most common), atrial flutter, SVT, VTach (especially Torsades if hypomagnesemic/hypokalemic)
Metabolic abnormalities of etoh withdrawal and how to manage
• alcoholic ketoacidosis
■ AG metabolic acidosis, urine ketones, low glucose, and normal osmolality
■ history of chronic alcohol intake with abrupt decrease/cessation
■ malnourished, abdominal pain with N/V
■ treatment: dextrose, thiamine (100 mg IM/IV prior to dextrose), volume repletion (with NS)
■ generally resolves in 12-24 h
Metabolic abnormalities associated with non etoh alcohols
• other alcohols ■ ethylene glycol CNS, CVS, renal findings
■ methanol
◆ early: lethargy, confusion
◆ late: headache, visual changes, N/V, abdominal pain, tachypnea
■ both ethylene glycol and methanol produce severe metabolic acidosis with anion gap (as the alcohol is metabolized) and osmolar gap (initially after ingestion but before metabolism)
What is potective with non etoh alcohol consumption
EtOH co-ingestion is protective
non etoh alcohol metabolic abnormality management
◆ urgent hemodialysis required
◆ fomepizole 15 mg/kg IV bolus OR EtOH 10% IV bolus and infusion to achieve blood level of 22 mmol/L (EtOH loading may be done PO)
consider folic acid for methanol, and pyridoxine and thiamine for ethylene glycol – both help reduce conversion to active metabolites
Alcohol associated GI abnormalities
Gastritic - common cause of abdominal pain and GI bleed in chronic alcohol users
• pancreatitis
■ serum amylase very unreliable in patients with chronic pancreatitis, may need serum lipase
■ hemorrhagic form (15%) associated with increased mortality
■ fluid resuscitation very important
• hepatitis
■ AST/ALT ratio >2 suggests alcohol as the cause as well as elevated GGT with acute ingestion
• peritonitis/spontaneous bacterial peritonitis
■ leukocytosis, fever, generalized abdominal pain/tenderness
■ occasionally accompanies cirrhosis
■ paracentesis for diagnosis (common pathogens: E coli, Klebsiella, Streptococcus)
• GI bleeds
■ most commonly gastritis or ulcers, even if patient known to have varices
■ consider Mallory-Weiss tear secondary to retching
■ often complicated by underlying coagulopathies
■ minor: treat with antacids
■ severe or recurrent: endoscopy
Methanol, ethylene glycol tox disposition
delayed onset, admit and watch clinical and biochemical marker
TCAs tox disposition
■ prolonged/delayed cardiotoxicity warrants admission to monitored (ICU) bed
■ if asymptomatic and no clinical signs of intoxication: 6 h ED observation adequate with proper decontamination and no ECG abnormalities
■ sinus tachycardia alone (most common finding) with history of overdose warrants observation in ED
Hydrocarbons/smoke inhalation dispo
■ pneumonitis may lag 6-8 h
■ consider observation for repeated clinical and radiographic examination
ASA, acetaminophen tox dispo
■ if borderline level, get second level 2-4 h after first
■ for ASA, must have at least 2 levels going down before discharge (3 levels minimum)
Oral hypoglycemic tox dispo
■ admit all patients for minimum 24 h if hypoglycemic and 12 h after last octreotide dose
■ observe asymptomatic patient for at least 8 h