Management of Office Emergencies Fernando Vega, M.D. - - PDF document

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Management of Office Emergencies Fernando Vega, M.D. 1

Fernando Vega, M.D.

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Classic Presentation Initially: prutitus, urticaria Angioedema, swelling f/b: respiratory Sx – stridor, dyspnea, wheeze Other Presentations Nausea, cramps, diarrhea, vomiting

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Management of Office Emergencies Fernando Vega, M.D. 2

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Management of Office Emergencies Fernando Vega, M.D. 3

Presence of an allergic sign (urticaria….) Involvement of at least two organ systems Exposure to agent or activity known to… Absence of condition that can mimic

anaphylaxis Skin

Angioedema, flushing, urticaria, pruritus

Cardiovascular

Tachycardia, palpitations, arrhythmias, hypotension,syncope

Gastrointestinal

Nausea, vomiting diarrhea, cramps

Respiratory

Dyspnea, stridor, wheezing, chocking, rhinorrhea,

Other

Sense of impending doom, diaphoresis, metallic taste

Urticaria Hyperventilation Vasovagal reaction Globus hystericus Hereditary angioedema Scromboid poisoning 0.3 – 0.5 cc epinephrine 1:1000

intramuscularly

May repeat every 15 minutes if necessary Diphenhydramine after epi Glucocorticosteroids after that:

Predinsone 40-60mg/day……

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Management of Office Emergencies Fernando Vega, M.D. 4

  • Persistent bronchospasm
  • Hypotension
  • Hypoxia
  • Patient is on beta-blockers
  • 20% of reactions are “biphasic” with

further mediator release 4 – 8 hours later. Most common causes of anaphylaxis include:

Drugs (particularly beta-lactams, NSAIDS, ACE inhibitors) Hymenoptera (bees, wasps) Radiographic contrast media Blood products Foods (particularly seafood, milk, nuts) 5 foods responsible for more than ¾ of food reactions in children:

Eggs (36%) Peanuts (24%) Cow’s milk (8%) Mustard (6%) Cod (4%)

Fin fish and shellfish more common in adults Children outgrow sensitivities to milk, eggs, soy but not usually to peanuts, nuts or fish Fatalities most common in teens following ingestion of peanuts or tree nuts

Anaphylaxis is not automatic on recurrent exposure:

40-60% on insect stings 20-40% on contrast media 10-20% on penicillin

Concurrent use of beta-blockers is a risk for severe prolonged anaphylaxis

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Management of Office Emergencies Fernando Vega, M.D. 5

Immediate Posibilities: Asthma Pulmonary Embolus Hyperventilation Anaphylaxis Foreign Body Obstruction Cardiac asthma Respiratory System Bronchospasm Pulmonary Embolus Pneumothorax Pulmonary infection Upper airway obstruction: aspiration, anaphylaxis Cardiovascular System Acute myocardial ischemia Congestive Heart Failure Cardiac tamponade If you hear hoof beats: asthma or

hyperventilation

No strange pain No strange history No strange physical findings History Previous episodes, outcomes Relative to current episode: How serious? How anxious? How long? Tired? Co-morbid conditions: CHF Hypertension (use of beta-blockers)

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Management of Office Emergencies Fernando Vega, M.D. 6

Physical Examination Started when you first looked at patient Level of anxiety Ability to complete sentences Accessory breathing:

Position of hands Pursed lips Accessory muscles

Physical Examination Wheezes No wheezes Air movement Pulse ratePulsus paradoxus – 12 mm Hg Δw/ inspr Laboratory Assessment Peak Flow meter

A fall of 50% from baseline is considered severe Hypercapnea happens only when PF falls below 20 percent Spirometry Demonstration Oxygen Saturation Meter

Initial treatment Inhaled albuterol 2nd best: OTC sympathomimmetics MDI w/spacer vs. updraft Followed by: Ipratropium bromide

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When to use steroids Less than 10% improvement in PEFR after first dose

  • f inhaled beta agonist

Less than 70% improvement of PEFR after first hour

  • f treatment

An asthma attack that developed in spite of steroids Protracted course How to use steroids As a rule 40 – 80 mg Prednisone qd Equivalent to 200 – 400 mg Hydrocortisone May taper, may not IV steroids for severe cases How to use steroids The effect of a single dose of oral prednisone begins

within 3 hours and reaches a maximum within 8-12 hours

In a study of 15, 40 and 125 mg of

methylprednisolone q6h of patients in status asthmaticus

125mg group got better end of first day 40mg group got better by middle of second day Inhaled steroids are for chronic use only

Pulmonary Embolus Sudden onset, Pleuritic pain and dyspnea Aortic dissection Tearing pain with radiation to back Pericarditis Positional ache, dyspnea Pneumothorax Pleuritic pain and dyspnea Acute coronary syndrome Vague, pressure-like pain, radiating to arm, neck, jaw

Chest Wall Pain Pleuritic Pain Visceral Pain

Costochondritis Pulmonary Embolus Exertional angina Precordial catch Pneumothorax Unstable angina Slipping rib Pericarditis Pericarditis Xyphodynia Pleurisy Aortic dissection Fibromyalgia Esoph reflux or spasm Gall bladder Pain Acute MI

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Management of Office Emergencies Fernando Vega, M.D. 8

Worst Case For patient (when you know the diagnosis) For Doctor (when you don’t know the Dx)

Acute Coronary Syndromes: Myocardial Ischemia and Infarction Acute Coronary Syndromes: Myocardial Ischemia and Infarction

Ischemic/anginal pain is similar to AMI pain AMI pain resolves with aggressive intervention Ischemic/anginal pain resolves with rest or

NTG

Acute Coronary Syndromes: Myocardial Ischemia and Infarction

Severe, deep pain Pain radiates to jaw or arm Gesture of resignation

Acute Coronary Syndromes: Myocardial Ischemia and Infarction

Visceral pain induces autonomic responses:

nausea, vomiting, diaphoresis

“Like an elephant stepping on my chest” Gesture of resignation

Acute Coronary Syndromes: Myocardial Ischemia and Infarction

Can be silent pain

Especially in diabetics Elderly Women

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Acute Coronary Syndromes: Myocardial Ischemia and Infarction

15 – 20 % AMI have some CHF Papillary muscle rupture in 1-3 days Pericarditis in 20% in 2-4 days Dysrhythmias occur in 72 – 100% of AMI

Acute Coronary Syndromes: Myocardial Ischemia and Infarction

Dysrhythmias occur in 72 – 100% of AMI

Acute Coronary Syndromes: Management

Direct admission to CCU (New information)

Acute Coronary Syndromes: Management

Direct admission to CCU Antiplatelet drugs:

ASA 160 – 325mg PO (↓ mortality by 23%) Clopidrogel 300mg loading f/b 75mg qd (more benefit)

Antithrombin drugs:

Heparin LMWH

Fibrinolytic Agents (for STEMI) Coronary reperfusion

Acute Coronary Syndromes: Management

Direct admission to CCU Other anti-ischemic therapies:

Nitroglycerin Morphine Metoprolol Atenolol

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In the absence of structural heart disease,

palpitations are overwhelmingly benign when the ECG is normal.

Not Atrial Fibrilation Not prolonged QT interval Not Torsade de Pointes

In the absence of structural heart disease,

palpitations are overwhelmingly benign

If they need to be treated, they will

complain

If they complain, they need to be treated

In the absence of ACS, palpitations are

  • verwhelmingly benign

Even NSVT = 4% of population In 60 – 85 year olds with no structural heart

disease followed for 10 years NSVT did not predict a coronary event

What do non-benign arrhythmias look like?

Not normal ECG

Atrial fibrilation, flutter Prolonged QT Most common complaint in ER

Location, quality, severity, onset, duration,

aggravating and alleviating factors

Absent bowel tones are not clinically useful

findings

Hyperactive or obstructive sounds are more

helpful

Rebound tenderness or “cough pain” is very

useful

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Non specific abdominal pain 34% Appendicitis 28% Biliary tract disease 10% Small Bowel Obstruction 4% Acute Gynecological disease 4% Pancreatitis 3% Renal Colic 3% Diverticular disease 2%

1800 pts, WBC >10k doubled odds of appendicitis

1800 pts, WBC <10k halved the odds of

appendicitis

Same with acute cholecytstitis In NSAP 28% of WBC counts >10.5K

Peptic Ulcer bleed accounts for 60% of Upper GI

bleeding Followed by erosive gastritis and esophagitis Followed by variceal bleeding Followed by Mallory Weiss

Hemmorrhoids are by far the most common cause of

lower GI bleeding Followed by diverticular bleeding, AVM, IBD,

and polyps

Both UGI LGI bleeding more common in ♂ Diarrhea is the most important differentiating

symptom

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Management of Office Emergencies Fernando Vega, M.D. 12

How High? How quickly did it get high? Symptoms of acute hypertensive effects? Symptoms of end organ damage?

An acute hypertneisve episode is defined as SBP > 180 and DBP > 110

Brain Severe HA, nausea, vomiting, altered sensorium, CVA Heart Ischemic symptoms Kidneys Proteinurea, hematuria, azotemia Vascular Aneurysm End organ dysfunction makes it an urgency Should have a glucose monitor in the office Should have urinalysis sticks in the office Hyper or hypoglycemia? Ketotic or non ketotic? Catch first presentation of diabetes Ongoing management of diabetes

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Not so common in office setting Caveat with sulfonylureas

Sweating Shakiness Anxiety Nausea Dizziness Confusion Blurred vision Headache Lethargy Typical symptoms

Typical Signs

Diaphoresis Tachycardia Almost any neurological finding

Altered mental status Tremor Focal Neurologic deficit Seizure

Management

Oral Glucose IV D50 1gm/kg f/b continuous drip Glucagon 1mg IM if IV access unavailable Hydrocortisone 100mg IV or glucagon 1mg IV

if hypoglycemia is refractory to glucose administration

Octreotide for refractory cases due to

sulfonylureas Management

Review co-morbid conditions Review social situation Most diabetics with insulin reactions respond

rapidly to treatment

Patients with prolonged or recurrent

hypoglycemia from sulfonylureas need to be admitted Ketosis on UA or not? How high is too high?

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Ketosis changes the whole clinical picture. Metabolic derangements are far more reaching and precipitous with ketosis.

Occurs predominantly in insulin dependent Mortality is 5% and is higher in elderly New onset diabetes presents as DKA in 25%

  • f cases

Precipitated by non-compliance with insulin

therapy or any type or physiologic stress such as:

infection Stroke MI pregnancy

Clinical Picture directly related to metabolic

derangements

Hyperglycemia causes osmotic diuresis

→dehydration, hypotension, tachycardia

Ketonemia causes acidosis with myocardial

depression, vasodilation and Kussmaul’ s

Clinical Picture Admit to hospital Correct Hypovolemia Correct Electrolyte abnormalities Correct Acidosis and ketonemia Treat underlying cause Management Is a common presentation of new-onset

diabetes mellitus

Occurs in poorly controlled type II DM Contraction alkalosis f/b metabolic acidosis Pathophysiology

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Typical patient is elderly with complaints of

weakness or mental status changes

Physical exam: dehydration and altered

mental status

Can have focal deficits or seizures Clinical Features Glucose > 600mg/dL HCO3 > 15 mg/dL pH > 7.3 Ketosis absent or mild Clinical Features Admit Correct hypovolemia Correct free water deficit HCO3 > 15 mg/dL pH > 7.3 Ketosis absent or mild Management

Rectal Temp > 38°C (100.4°F) Priority is to identify the child with a serious bacterial illness

The higher the fever, the higher incidence of

bacteremia

Age 0-8 weeks at high risk of SBI Highest risk for sepsis first few days of life Infants 0- 3 months

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The higher the fever, the higher incidence of

bacteremia

Age 0-8 weeks at high risk of SBI Highest risk for sepsis first few days of life Age 0-8 week infant may have Bacterial

Sepsis w/o clinical findings

Febrile infants < 4 weeks 13% incidence Febrile infants < 8 weeks 10% incidence Infants 0- 3 months Clinical impression is more reliable in this group Viral illnesses including pneumonia account for

the most common etiology

Strep pneumoniae is the most common bacterial

etiology

.019% of bacteremia develop meningitis Infants 3-24 months

Indications for Admission to Hospital All infants <4 weeks with T> 38.1°C (100.6°F) Most infants <3 moths with focal infection

  • ther than otitis media

Toxic appearance regardless of age or degree

  • f fever

Occurs typically Oct – May Infants less than 2 years, peak at 2 mo Increased risk of complications

Prematurity BPD Congenital Heart

Epidemiology Begins with nasal discharge, pharyngitis,

cough and fever

Wheezing and respiratory distress follow

later.

Tachypnea, nasal flaring and grunting Ominous signs of RF: Decrease or absence

  • f breath sounds signifies severe

bronchocnstriction

Clinical Features Symptoms peak in 3-5 days Usually resolve in 2 weeks Immunity is variable Reinfection may occur Clinical Features

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May respond to albuterol but probably not. Nebulized epinephrine may be helpful Heliox may be helpful Hydration Steroids Management Indications for hospitalization

Apnea Respiratory distress unresponsive to Tx Hypoxia Vomiting or dehydration Tachypnea > 60

Management Clinical Features Life threatening Can occur at any age Abrupt onset of High fever, sore throat,

stridor, dysphagia and drooling over 2 d.

Severe sore throat with normal appearing

  • ropharynx.

X-rays are unnecessary Lifetime likelihood of one Sz is 9% Age 0-9 years prevalence is 4.4/1000 Age 10-19 yrs prevalence is 6.6/1000 Simple febrile Sz are a different category with

incidence of 3-4%

Clinical Features Symptoms can be any of the following:

Alteration of consciousness Auditory, sensory or olfactory hallucinations Involuntary motor activity Choreoathetoid movements

Clinical Features Neonatal seizures may be subtle and

sometimes w/ only autonomic changes:

Mydriasis Apnea Cardiac irregularity

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A convulsion associated with an elevated

temperature greater than 38ºC

A child younger than six years of age No central nervous system infection or

inflammation

No acute systemic metabolic abnormality that

may produce convulsions

No history of previous afebrile seizures Seizures that last less than 15 minutes Have no focal features If they occur in a series, the total duration is

less than 30 minutes

Last more than 15 minutes Have focal features or postictal paresis Occur in a series with a total duration greater

than 30 minutes.

Meningitis and encephalitis are the main concerns in a child presenting with fever and seizures. .

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Management of Office Emergencies Fernando Vega, M.D. 19

Know mechanism of injury Check neurovascular status General fracture care:

Ice, traction, splinting

Special Fractures:

Scaphoid Radial head Metatarsal shaft Ankle dome

Abcesses Bite wounds Wound management

“Golden Rule” of 8 hours Neurovascular exam

Mechanism of injury will help identify risk of

foreign body, contamination and wound complication

Crush injuries more likely to cause wound

infection

Hematomas often require drainage History of prodrome Post-ictal phenomenon Memory of the event Witnesses Differentiation syncope from seizures Subconjunctival hemorrhage Trauma: check integrity and acuity Corneal Foreign body Corneal abrasion Acute angle closure glaucoma Testicular Torsion Urinary retention Epididymitis

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Menorrhagia Threatened abortion

20-40% of pregnancies abort spontaneously Chromosomal abnormalities account for most

Dysfunctional Uterine Bleeding Ectopic Pregnancy

Pneumothorax Burns Wound care Head injuries Poisonings