Respiratory Distress
A.
Dyspnea
B.
C.
A.
B.
C.
D.
Hypoxia
A.
Urgent Care
Respiratory Failure/Arrest (TEMM)
Respiratory Failure: Defined as respiratory dysfunction resulting in
abnormalities of oxygenation or ventilation severe enough to threaten
function of vital organs
Causes are multifactorial
Findings: dyspnea, hypoxia, hypercapnia, and cyanosis
Definition: subjective feeling of difficult, labored, or uncomfortable
breathing; most pts w dyspnea have cardio or pulmonary cause
Clinical Findings
1. Initial assessment should be directed toward identifying respiratory
failure
a. Significant respiratory distress: tachycardia, tachypnea, stridor,
and use of accessory muscles; lethargy, agitation, AMS, inability to
speak d/t breathlessness
i.
Administer O2 immediately
ii.
No improvement -> anticipate need for aggressive airway
management and mechanical ventilation
b. Lack of these signs and symptoms -> detailed H&P to determine
cause of dyspnea
Diagnosis and Differential
1. Diagnostic Testing (to determine etiology)
a. Pulse Ox
b. CXR
c. Peak Flow
d. EKG, Cardiac Enzymes
e. Labs: ABG, CBC, BNP, D-dimer, Cardiac Enzymes
f. Other special testing (CT of chest, echo, stress test, PFTs, etc)
2. Differential:
a. Most Common Causes: COPD/Asthma, CHF, Ischemic Heart Disease
(unstable angina and MI), Pneumonia
b. Most Immediately Life-Threatening: upper airway obstruction (FB,
angioedema, hemorrhage), tension pneumothorax, pulmonary
embolism, neuromuscular weakness (myasthenia gravis, GuillainBarre, botulism)
Emergency Department Care and Disposition
1. Impending Respiratory Failure -> aggressive airway management and
mechanical ventilation; consider non-invasive ventilation techniques
(CPAP and BiPAP)
2. Goal of Therapy: PaO2 > 60 mm Hg or O2 saturation > 90%; lower goals
appropriate for those w long standing lung disease (COPD)
3. Disposition: any patient with hypoxia and unclear cause of dyspnea
requires hospital admission
General Considerations
1. Definition: inadequate delivery of oxygen to the tissues
2. O2 delivery is a function of: cardiac output, hemoglobin concentration,
and oxygen saturation
3. Hypoxemia – PaO2 < 60 mm Hg
a. Results form combo of 5 distinct mechanisms
i.
Hypoventilation -> inc PaCO2 displaces oxygen from
B.
C.
D.
Hypercapnia
A.
B.
C.
alveolus lowering amount of O2 delivered to the capillaries
ii.
Right to Left Shunt - blood bypasses lungs thereby inc
amount of unoxygenated blood entering systemic circulation
iii.
Ventilation/Perfusion Mismatch – areas of lung are perfused
but not ventilated
iv.
Diffusion Impairment – alveolar blood barrier abnormality
causes impairment of oxygenation
v.
Low inspired oxygen (such as at hi altitudes)
Clinical Features
1. S/Sx: non-specific
a. Chief symptom is dyspnea (CMDT)
b. Signs: cyanosis, restlessness, confusion, anxiety, delirium,
tachypnea, bradycardia or tachycardia, HTN, tremor (CMDT)
2. Physiologic Response:
a. Pulmonary arterial vasoconstriction + inc in minute ventilation and
sympathetic tone -> tachypnea, tachycardia, initial hyperdynamic
cardiac state
b. Predominant features can be neurologic: HA, somnolence, lethargy,
anxiety, agitation, coma, or seizures
c. Chronic Hypoxemia: polycythemia, clubbing, cor pulmonale, change
in body habitus (pink puffer/blue bloater of COPD)
Diagnosis and Differential
1. Formal diagnosis requires ABG
2. Etiology: multifactorial
3. Clues to etiology can be obtained by calculating the Alveolar-arterial
oxygen gradient (A-a gradient)
a. A-a gradient inc in cases of right to left shunts, V/Q mismatch, and
diffusion impairment
Emergency Department Care and Disposition
1. Supplemental O2 to achieve O2 saturation > 90%
2. Manage airway aggressively as needed
3. Cause specific treatment and evaluation should be pursued
4. All patients with new hypoxemia should be admitted and monitored
until condition is stable
General Considerations
1. PaCO2 > 45 mm Hg
2. Exclusively d/t alveolar hypoventilation
3. Factors affecting alveolar ventilation: respiratory rate, tidal volume,
and dead space volume
Clinical Features
1. Acute elevations result in increased ICP -> HA, confusion, and lethargy;
coma, encephalopathy, and seizures may be present when PaCO2 rises
above 80 mm Hg
2. Cardinal Symptom: Dyspnea & HA (CMDT)
3. Signs: peripheral and conjunctival hyperemia, HTN, tachycardia,
tachypnea, impaired consciousness, papilledema, asterixis (CMDT)
Diagnosis and Differential
1. ABG required for diagnosis; pulse ox may be completely normal
2. Common Causes: COPD, respiratory center depression from drugs
(opiates, sedatives, anesthetics), neuromuscular impairment (GuillainBarre, botulism), thoracic cage disorders (morbid obesity,
D.
Cyanosis
A.
B.
C.
kyphoscoliosis)
Emergency Department Care and Disposition
1. Aggressive measures to inc minute ventilation
2. Airway maintenance is crucial and mechanical ventilation may be
indicated
3. A trial of BiPAP or CPAP; some cases should included disease specific
therapies (bronchodilators for COPD, reversal for opiate overdose)
4. Disposition depends on etiology; many require hospital admission and
monitoring
General Considerations
1. Bluish color of the skin or mucous membranes resulting from inc
amount of deoxyhemoglobin
2. Cyanosis usually present when deoxyhemoglobin level exceeds
5mg/dL
3. Presence suggests tissue hypoxia
4. Very subjective
Clinical Features
1. Cyanosis w normal PaO2 suggests and abnormal hemoglobin such as
methehemoglobin
2. Central
a. Under tongue and on buccal mucosa
b. Inadequate pulmonary oxygenation or abnormal hemoglobin
3. Peripheral
a. Distal extremities
b. Diminished peripheral blood flow
Diagnosis and Differential
1. ABG analysis with cooximtry is gold standard
a. Pulse Ox – good for continuous monitoring, may overestimate
oxygen saturation when there is dyshemoglobinemia
b. ABG – alone may be misleading in presence of abnormal
hemoglobin
i.
Methehemoglobin – associated with blood that is “chocolate
brown” and does not change color when exposed to room
air
ii.
Carboxyhemoglobin – cherry red mucous membrane
discoloration
2. Hematocrit – may reveal a polycythemia vera or severe anemia both of
which may contribute to cyanosis
3. Differential
a. Central
i.
Hypoxemia
- Dec FiO2: hi altitude
- Hypoventilation
- Ventilation/perfusion mismatch
- Right to left shunt (congenital heart disease, pulmonary
AV fistulas, multiple intrapulmonary shunts)
ii.
Hemoglobin Abnormalities
-Methehemoglobinemia: hereditary, acquired
- Sulfhemoglobinemia: acquired
- Carboxyhemoglobinemia: not true cyanosis
b. Peripheral
Altered Mental
Status in Children
i.
Reduced cardiac output
ii.
Cold extremities
iii.
Mal-distribution of blood flow: distributive forms of shock
iv.
Arterial or Venous Obstruction
D. Emergency Department Care and Disposition
1. Supplemental O2 to achieve O2 saturation > 90%
a. Those with central cyanosis should improve rapidly
b. If no improvement -> suspect impaired cardiac circulation,
abnormal hemoglobin, or pseudocyanosis
2. Peripheral cyanosis should respond to therapy directed at specific
condition causing the cyanosis
Deteriorating Mental Status/Unconscious Patient (TEMM)
A. General Considerations
1. Definition: failure to respond to the external environment in a manner
consistent with the child’s developmental level after appropriate
stimulation
B. Clinical Features
1. Spectrum: confusion, lethargy, stupor, coma indicative of depression of
the cerebral cortex or localized abnormalities of the reticular activating
system
2. AVPU Scale – simplified and functional coma scale
a. A = alert; GCS of 15
b. V = responsive to verbal stimuli; GCS of 13
c. P = responsive to painful stimuli; GCS of 8
d. U = unresponsive; GCS of 3
3. Pathologic Conditions Affecting Mental Status
a. Supratentorial lesions – altered level of consciousness and focal
motor abnormalities w a rostral to caudal progression of
dysfunction, slow nystagmus toward the stimulus during cold
caloric testing
b. Subtentorial lesions – rapid loss of consciousness, cranial nerve
abnormalities, abnormal breathing patterns, and asymmetric or
fixed pupils
c. Metabolic Encephalopathy – dec level of consciousness before
exhibiting motor signs, which are symmetrical when present;
pupillary reflexes are intact except with profound anoxia, opiates,
barbiturates, and anticholinergics
C. Diagnosis and Differential
1. Thorough H&P
a. Hx:
i.
Prodromal events/associated signs and symptoms: fever,
HA, weakness, vomiting, diarrhea, gait disturbances, head
tilt, rash, palpitations, abdominal pain, hematuria, and wt
loss
ii.
PMH, Family Hx, Immunization status
b. PE: look for signs of occult infection, trauma, toxicity, metabolic
disease (AEIOU TIPS mnemonic)
2. Diagnostic Adjuncts: bedside glucose, analysis of blood, gastric fluid,
urine, stool, CSF, EKG, radiographs…guided by clinical situation
D. AEIOU TIPS mnemonic for pediatric AMS
1. A
2.
3.
4.
5.
6.
7.
8.
9.
a. Alcohol - changes in mental status can occur with serum levels
<100 mg/dL; concurrent hypoglycemia is common
b. Acid-Base and Metabolic – hypotonic and hypertonic dehydration.
Hepatic dysfunction, inborn errors of metabolism, DKA, primary
lung disease, and neurologic dysfunction causing hypercapnia
c. Arrhythmia/Cardiogenic – Stokes-Adams, SVT, aortic stenosis,
heart block, VFib, pericardial tamponade
E
a. Encephalopathy – hypertensive encephalopathy can occur with
diastolic pressure of 100-110 mm Hg. Reye syndrome. HIV. Postimmunization encephalopathy. Encephalomyelitis
b. Endocrinpathy – Addison disease can present w AMS or psychosis.
Thyrotoxicosis can present w ventricular dysrhythmias.
Pheochromocytoma can present w hypertensive encephalopathy
c. Electrolytes – hyponatremia becomes symptomatic around 120
mEq/L. Hypernatremia and disorders of calcium, magnesium, and
phosphorus can produce AMS
I
a. Insulin – AMS from hyperglycemia is rare in children, but DKA is
the most common cause. Hypoglycemia can be the result of many
disorders. Irritability, confusion, seizures, and coma can occur with
blood glucose levels <40 mg/dL
b. Intussusception – AMS may be the initial presenting symptom
Opiates – common household exposures are to Lomotil, Imodium,
diphenoxylate, and dextromethorphan. Clonidine, and alpha agonist,
can also produce similar symptoms
Uremia – encephalopathy occurs in over one third of patients with
chronic renal failure. Hemolytic uremic syndrome can produce AMS in
addition to abdominal pain. Thrombocytopenic purpura and hemolytic
anemia also can cause AMS.
T
a. Trauma – children with blunt trauma are more likely than adults to
develop cerebral edema. Look for signs of child abuse, particularly
shaken baby syndrome with retinal hemorrhages.
b. Tumor – Primary, metastatic, or meningeal leukemic infiltration.
c. Thermal – Hypo or Hyperthermia
I
a. Infection – one of the most common causes of AMS in children.
Meningitis should be considered, particularly in febrile children
b. Intracerebral vascular disorders – subarachnoid, intracerebral or
intravascular hemorrhages can be seen with trauma, ruptured
aneurysm, or AV malformations. Venous thrombosis can follow
severe dehydration or pyogenic infection of the mastoid, orbit,
middle ear, or sinuses.
P
a. Psychogenic – rare in the pediatric age group, characterized by dec
responsiveness with normal neuro exam including oculovestibular
reflexes
b. Poisoning – drugs or toxins can be ingested by accident, through
neglect or abuse, or in a suicide gesture
Seizure – generalized motor seizures are often associated with
E.
Delirium
A.
B.
C.
prolonged unresponsiveness in children. Seizures in young febrile
patient suggest intracranial infection. Shunt malfunction should be
considered among patients with a ventriculoperitoneal shunt for
hydrocephalus
Emergency Department Care and Disposition (stabilize and reverse lifethreatening conditions)
1. ABCs; immobilize cervical spine if trauma suspected and obtain
appropriate radiographic studies when pt is stable
2. Continuous pulse ox and supplemental oxygen as needed to correct
hypoxia, including BVM and intubation with capnography when
appropriate.
3. Fluid resuscitation – 20 mL/kg fluid bolus of isotonic crystalloid for
hypotension; repeat upt to 60 mL/kg, after which uses pressors
(dopamine)
4. Hypoglycemia – 10% dextrose 4-5 mL/kg in infants or 25% dextrose 2
mL/kg in older children
5. Control core body temp to minimize metabolic demands.
6. Seizures – use benzos
7. Opiate/Clonidine OD – naloxone (0.01-0.1 mg/kg IV every 2 min)
8. Benzo OD – Flumezenil (0.01 mg/kg IV)
9. Meningitis - Empiric abx (ceftriaxone or cefotaxime 50 mg/kg/dose)
and consider vacomycin 10 mg/kg/dose
10. Most patients will require admission and extended observation
General Considerations
1. Mental Status – clinical state of emotional and intellectual functioning
of the individual.
2. AMS in the Urgent Care/ED – delirium, dementia, and coma
Clinical Features
1. Transient disorder characterized by impaired attention, perception,
memory, and cognition
2. Sleep-wake cycles may be disrupted – inc somnolence during the day
and agitation at night (sundowning)
3. Alertness is reduced
4. Activity levels may fluctuate rapidly
5. Other S/Sx: tremor, asterixis, tachycardia, sweating, HTN, emotional
outbursts, and hallucinations
Diagnosis and Differential
1. Acute onset of attention deficits and cognitive abnormalities
fluctuating throughout the day and worsening at night is virtually
diagnostic
2. Detailed med hx
3. Look for underlying process such as infection
4. Ancillary tests: BMP, hepatic studies, UA, CBC, and CXR, cranial CT if
mass lesion suspected, LP if meningitis or SAH suspected
5. DDx:
a. Infectious: pneumonia, UTI, meningitis/encephalitis, sepsis
b. Metabolic/Toxic: hypoglycemia, alcohol ingestion, electrolyte
abnormalities, hepatic encephalopathy, thyroid disorders, alcohol
or drug withdrawal
c. Neurologic: stroke/TIA, seizure or postictal state, SAH, intracranial
hemorrhage, CNS mass lesion, subdural hematoma
D.
Dementia
A.
B.
C.
Coma
A.
d. Cardiopulmonary: CHF, AMI, PE, Hypoxia or CO2 narcosis
e. Drug-related: Anticholinergic drugs, alcohol or alcohol withdrawal,
sedatives-hypnotics, narcotic analgesics, polypharmacy
Emergency Department Care and Disposition
1. Tx underlying cause
2. Tx agitation with haloperidol, 5-10 mg PO, IM, or IV w reduced dosing
of 1-2 mg in elderly. Lorazepam, 0.5-2mg PO, IM, or IV may be used in
combo w Haldol
3. Admit unless reversible cause discovered, tx initiated, and
improvement seen
Clinical Features
1. Loss of mental capacity
2. Psychosocial level and cognitive abilities deteriorate and behavioral
problems develop
3. Largest categories: Alzheimer disease and vascular dementia
4. Onset is insidious
5. S/Sx: hallucinations, delusions, repetitive behaviors, and depression
are common, as is impairment of memory, particularly recent memory
6. Other S/Sx: naming problems, forgetting items, loss of reading and
direction, disorientation, inability to perform self-care tasks, and
personality changes, anxiety, speech difficulties
7. S/Sx associated w Vascular Dementia: asymmetric DTRs, gait
abnormalities, or extremity weakness
Diagnosis and Differential
1. Alzheimer’s - develops slowly
2. Vascular Dementia – abrupt worsening; focal neuro signs; fluctuating,
stepped course
3. Parkinson’s – extrapyramidal signs
4. Diagnostic studies – CBC, BMP, UA, Thyroid profile, serum vitamin B12
level, testing for syphilis, ESR, serum folate, HIV, CXR, consider head
CT/MRI, LP if dx not readily apparent
5. DDx: delirium, depression, other treatable causes
Emergency Department Care and Disposition
1. Identify treatable causes
2. Antipsychotics to manage persistent psychosis or severely
disruptive/dangerous behavior; use is associated w adverse reactions
3. Aim tx of vascular dementia at addressing risk factors such as HTN
4. Consider normal pressure hydrocephalus if urinary incontinence and
gait disturbance are noted. This is further suggested by excessively
large ventricles on head CT. Consider LP with CSF drainage
5. Most patients w newly diagnosed dementia require admission for
further evaluation and treatment
Clinical Features
1. State of reduced alertness and responsiveness from which the patient
cannot be aroused
2. GCS
B. Diagnosis and Differentials
1. Abrupt -> stroke or seizure
2. Gradual -> metabolic process or progressive lesion (tumor or bleed)
3. Exam – look for trauma, toxidromes, focal signs (asymmetric findings
on pupillary exam, assessment of corneal reflexes, and testing of
oculovestibular reflexes, muscle tone)
4. Ancillary Testing – head CT, LP
5. DDx:
a. Coma from causes affecting the brain diffusely
i.
Encephalopathies
- Hypoxic Encephalopathy
- Metabolic Encephlopathy
~Hypoglycemia
~Hyperosmolar state (hyperglycemia)
~Electrolyte abnormalities (hyper/hyponatremia,
hypercalcemia)
~Organ System Failure
Hepatic encephalopathy
Uremia/renal failure
Endocrine (eg. Addison disease, hypothyroidism, etc)
Hypoxia
CO2 narcosis
-Hypertensive Encephalopathy
ii.
Toxins
iii.
Drug reactions (neuroleptic malignant syndrome)
iv.
Environmental causes – hypothermia, hyperthermia
v.
Deficiency State – Wernicke encephalopathy
vi.
Sepsis
b. Coma from primary CNS disease or trauma
i.
Direct CNS Trauma – diffuse axonal injury, subdural
hematoma, epidural hematoma
ii.
Vascular disease – intraparenchymal hemorrhage
iii.
Subarachnoid hemorrhage
iv.
Infarction – hemispheric, brainstem
v.
CNS Infections
vi.
Neoplasms
vii.
Seizures – non-convulsive status epilepticus, postictal state
C. Emergency Department Care and Disposition
1. Stabilize airway, ventilation, and circulation
2. Identify and tx reversible causes such as hypoglycemia and opioid
toxicity (naloxone, thiamine, and glucose)
3. If elevated ICP -> elevated head to 30*, Mannitol
Features of Delirium,
Dementia, and
Psychiatric Disorder
General
A.
B.
Clinical Features
A.
B.
C.
D.
Allergic Reaction/Anaphylaxis (TEMM)
Range from localized urticarial to life-threatening anaphylaxis
Anaphylaxis – most severe form of immediate hypersensitivity reaction;
encompasses both IgE-mediated reactions and anaphylactoid reactions,
which do not require a previous sensitizing exposure
Onset – may occur w/in seconds or be delayed over an hour after an
exposure; more rapid reactions are associated w higher mortality
Common Exposures: foods, medications, insect stings, and allergen
immunotherapy injections
Criteria for Anaphylaxis: acute progression of organ system involvement
that may lead to cardiovascular collapse
1. Organ system involvement can include:
a. Dermatologic – pruritus, flushing, urticarial, erythema multiforme,
angioedema
b. Respiratory Tract – dyspnea, wheezing, cough, stridor, rhinorrhea
c. Cardiovascular – dysrhythmias, collapse, arrest
d. GI – cramping, vomiting, diarrhea
e. GU – urgency, cramping
f. Eye – pruritus, tearing, redness
Biphasic mediator release
1. Can occur in up to 20% of cases
Diagnosis and
Differential
A.
B.
C.
D.
E.
Emergency
Department Care and
Disposition
A.
B.
C.
D.
E.
F.
G.
H.
I.
Clinical Features
A.
B.
C.
2. Recurrence of symptoms 4-8 hours after initial exposure
Clinical dx
Hx can confirm exposure to new drug, food, or sting
No specific test to verify dx in real time; consider in any rapidly
progressing multi-system illness
Work up – r/o other dx while stabilizing pt
Differential (depends on organ system involved): myocardial ischemia,
gastroenteritis, asthma, carcinoid, epiglottitis, hereditary angioedema,
vasovagal reactions…
ABCs; cardiac monitor w pulse ox, IV access
Oxygen as indicated by oximetry; angioedema or respiratory distress
should prompt early consideration for intubation
Limit further exposure (stop drug, remove stinger…); First aid measures,
ice, and elevation may be helpful for local symptoms
First line therapy: epi (0.3-0.5mg IM in the thigh); refractory to IM or in
shock -> IV epi
Hypotensive -> aggressive fluid resuscitation w normal saline (1-2L)
Steroids should be used in all cased to control persistent or delayed
reactions; severe -> IV methylprednisolone; mild -> prednisone
Antihistamines: Diphenhydramine 50 mg IV +/- Ranitidine 50 mg IV
Bronchospasm -> albuterol nebulizer; if refractory, consider ipratropium
bromide and magnesium
Disposition
1. Unstable or refractory –> ICU admission
2. Moderate to severe -> admit for observation
3. Mild -> observed in ED (~4 hrs), sent home if symptoms are
stable/improving
4. Discharge patients on an antihistamine and short course of prednisone
5. Counsel patients about late recurrence of symptoms, avoiding further
exposures, and access to and use of epi pen
6. If severe, consider Medic-Alert bracelets and referral to an allergist
Acute Abdomen (TEMM)
Consider immediate life threats that might require emergency
intervention
Hx
1. Time of pain onset, character, severity, location of pain and its referral,
aggravating and alleviating factors, similar prior episodes
2. ROS: CV (chest pain, dyspnea, cough), GU (urgency, dysuria, vaginal
discharge), trauma
3. Older Patients: hx of MI, dysrhythmias, coagulopathies, vasculopathies
4. PMH and Sx Hx
5. Medications: steroids, abx, NSAIDs
6. Females: thorough GYN hx
PE
1. General appearance
a. Peritonitis – lie still
2. Vitals – signs of hypovolemia (blood loss, volume depletion)
a. Tachycardia may not always occur in face of hypovolemia
b. Absence of fever does not r/o infection, particularly in the elderly
3. Skin – pallor, jaundice
D.
Diagnosis
A.
B.
C.
D.
E.
Differential
A.
B.
C.
D.
E.
4. Abdomen
a. Inspection – contour, scars, peristalsis, masses, distention,
pulsation
b. Auscultation – hyperactive or high-pitched bowel sounds = inc
likelihood of SBO
c. Palpation (most important) – tenderness, guarding, masses,
organomegaly, hernias; rebound tenderness (peritonitis)
5. Pelvic Exam in all postpubertal females
a. During rectal exam – assess for tenderness, bleeding, and masses
Caution in Elderly Patients – they fail to manifest same signs and
symptoms; dec pain perception and dec febrile or muscular response to
infection/inflammation
1. Biliary disease, bowel obstruction, diverticulitis, cancer, and hernia are
more common in patients over 50
2. Sigmoid volvulus, diverticulitis, acute mesenteric ischemia (pain out of
proportion to physical exam), and abdominal aortic aneurysm - less
frequent conditions but proportionately higher occurrence in elderly
Pregnancy Test – all women of child-breaing age with abdominal pain or
abnormal vaginal bleeding
CBC
Plain Xrays – look for obstruction, perforation (free air), stones
US – cholelithiasis, choledocholithiasis, cholecystitis, biliary duct
dilatation, pancreatic masses, hydroureter, intrauterine or ectopic
pregnancies ovarian and tubal pathologies, free intraperitoneal fluid,
suspected appendicitis, AAA
CT – mesenteric ischemia, pancreatitis, biliary obstruction, aortic
aneurysm, appendicitis, and urolithiasis; w IV contrast for vascular lesions
and inflammatory conditions (appendicitis); w/o for urolithiasis
Diffuse Pain - aortic aneurysm (leaking, ruptured), aortic dissection,
appendicitis (early), bowel obstruction, diabetic gastric paresis,
gastroenteritis, heavy metal poisoning, hereditary angioedema, malaria,
mesenteric ischemia, metabolic disorder (Addisonian crisis, DKA, uremia),
Narcotic withdrawal, pancreatitis, Perforated bowel, Peritonitis, sickle cell
RUQ – appendicitis (retrocecal), biliary colic, cholangitis, cholecystitis,
Fitz-Hugh-Curtis syndrome, hepatitis, hepatic abscess, hepatic congestion,
herpes zoster, myocardial ischemia, perforated duodenal ulcer,
pneumonia (RLL), pulmonary embolism
LUQ – gastric ulcer, gastritis, herpes zoster, myocardial ischemia,
pancreatitis, pneumonia (LLL), pulmonary embolism, splenic
rupture/distension
RLQ – aortic aneurysm (leaking, ruptured), appendicitis, crohns (terminal
ileitis), diverticulitis (cecal), ectopic pregnancy, endometriosis, epiploic
appendagitis, herpes zoster, inguinal hernia (incarcerated, strangulated),
ischemic colitis, meckel diverticulum, Mittelschmerz, ovarian cyst
(ruptured), ovarian torsion, PID, psoas abscess, testicular torsion, ureteral
calculi
LLQ – aortic aneurysm (leaking, ruptured), diverticulitis (sigmoid), ectopic
pregnancy, endometriosis, epiploic appendagitis, herpes zoster, inguinal
hernia (incarcerated strangulated) ischemic colitis, mittleschmerz, ovarian
cyst (ruptured), ovarian torsion, PID, psoas abscesss, regional enteritis,
testicular torsion, ureteral calculi
Emergency
Department Care and
Disposition
General
Skin Review
Depth of Burn
Classified According
to Degrees
1. IV hydration with NS or LR; keep NPO in case surgical candidate
2. Judicious use of analgesics – morphine 0.1 mg/kg IV; NSAIDs useful in
renal colic but controversial in other conditions d/t masking of peritoneal
inflammation
3. Antiemetics such as Ondansetron or metoclopramide IM/IV
4. Abx tx when appropriate (gentamicin + metronidazole or piperacillintazobactam) and depending on suspected source of infection
5. Sx or OBGYN consultation for patients w acute abdominal or pelvic
pathology requiring immediate intervention
a. The Acute/Surgical Abdomen – pain, guarding, rebound; indicate likely
need for emergent sx
6. Indications for admission: toxic appearance, unclear diagnosis in elderly,
intractable pain/vomiting, AMS…
Burns (PABR)
A. Classified into 6 grps based on mechanism of injury
1. Scalds
2. Contact burns
3. Fire
4. Chemical
5. Electrical
6. Radiation
B. Highest Incidence: first few years of life & btw ages 20-29
A. Epidermis
1. 4 specific layers
2. Function in protection from environment, water homeostasis, and
immunologic surveillance
B. Dermis
1. Type I Collagen is maj. of dermis
2. Contains pilosebaceous unit, apocrine gland, ecocrine gland, melanocytes,
nerve end organs and Merkel and Langerhans cells
3. Provides communication from the skin to the immunologic and nervous
syst.
C. Subcutaneous Tissue
1.Contains fat cells and provides a “cushion” for dermis
2. Thickness varies depending on total body fat.
A. First-Degree
1.Minor epithelial damage of epidermis
2. Redness, tenderness, and pain
3.No blistering, 2-point discrimination in tact
4. Healing takes several days & occurs w/o scarring
5. Most common causes: flash burns and sunburn
B. Second-Degree
1. Superficial Partial-Thickness Burn
a. Involves epidermis and superficial dermis layers
b. Skin appears pink, moist, and soft; thin-walled blisters are present
c. Skin is very tender to touch
d. Heals in 2-3 weeks, typically w/o scarring
2. Deep Partial-Thickness Burn
a. Involves the epidermis and extends into the lower (reticular) dermis
layer
C.
D.
Diagnosis
A.
B.
C.
Prehospital Care
A.
B.
Hospital Care
A.
b. Skin appears red w blanched white areas; thick-walled blisters
c. Heal in 3-6 weeks; scarring is possible w development of contractions
across jts.
3. Second degree typically d/t splash scalds
Third Degree
a. Full-thickness burn that destroys the full thickness of the epidermis and
dermis
b. Skin is white or leathery w underlying clotted vessels and destruction of
sensory nerve endings results in anesthesia of affected area
c. Skin grafting needed unless burn is small (<1cm in diameter)
d. Caused by immersion scalds, flame burns, chemical and high-voltage
electrical injuries
Fourth Degree
a. Full-thickness destruction of skin, subcutaneous tissue, fascia, muscles,
bone, & other structures
b. Tx requires debridement & reconstruction of tissues
c. Result from prolonged exposure to causes of 3rd degree burns
Burn Wound Assessment
1. Rules of Nines
a. Adult BSA
i.
9% head and neck
ii.
9% each upper extremity
iii.
18% anterior portion of trunk
iv.
18% posterior portion of trunk
v.
18% each lower extremity
vi.
1% perineum & genitalia
Carboxyhemoglobin
1. Carbon monoxide level should be obtained
2. Tx w 100% O2 until level less than 10%
a. Hyperbaric oxygen may be needed if presence of metabolic acidosis, hx
of neuro deficits, pregnancy, cardiac abnormalities, very young/old
Cyanide
1. Inhalation injury may lead to cyanide poisoning
2. Tx w nitrite-thiosulfate antidote
Evaluate for Sign of Inhalation Injury
1. Includes dyspnea, burns on mouth and nose, soot in posterior pharynx,
singed nasal hairs, sooty sputum, and cough
2. Tx w humidified oxygen, non-rebreathing mask at 10-12 L/min
All burned clothing and skin should be washed w cool water
1. Inhibits lactate production and acidosis
2. Limits vascular permeability
3. Dec dermal ischemia
Fluid Resuscitation
1. Tremendous fluid loss
2. Adequate fluid resuscitation is evidenced by normal urine output
a. 30-40 mL/hr in adults
3. Parkland formula for fluid resuscitation
a. Uses lactated Ringer’s solution
b. Total volume given is 4mL/kg/% BSA burned during first 24 hrs
i.
½ of total is given first 8 hrs; rest given over next 16 hrs
ii.
%BSA burned only includes 2nd & 3rd degree burns
Obstetric
Hemorrhage
Placenta Previa
B. Pain Management
1. Requirement for pain meds is inversely related to depth of burn injury
a. Full-thickness burns are painless, d/t sensory nerve damage
C. Escharotomy
1. Full-thickness circumferential burn of an extremity may result in vascular
compromise
2. May note loss of pulses and inc in tissue compartment pressure
3. Escharotomy prevents ischemic injury
Third Trimester Bleeding (Medicine Powerpoint)
A. Leading cause of maternal death
B. Major causes of antepartum hemorrhage include Placenta Previa and
Placental Abruption
A. General Considerations
1. Accounts for 20% of all antepartum hemorrhages
2. Abnormal implantation of placenta over the internal cervical os
a. Complete: covers the os
b. Partial: covers portion of the os
c. Marginal: at the edge of the os
d. Low Lying: implanted on lower uterine segment
B. Risk Factors
1. Prior C/S (C-section), uterine sx (ex: myomectomy)
2. Multiparity
3. Multiple gestation
4. Smoking
5. Hx of placenta previa
6. AMA
C. Fetal Complications
1. Preterm delivery
2. PROM
3. IUGR (growth restriction)
4. Malpresentation (breech or transverse)
5. Vasa previa (passes over int. os), velamentous cord insertion
6. Congeital abnormalities
D. Complications of Placenta Previa
1. Accreta: superficial attachment & invasion into uterine wall
2. Increta: invades myometrium
3. Percreta: penetrates myometrium to uterine serosa
E. Clinical Sx
1. Sudden profuse painless vaginal bleeding
2. If accreta, usually asymptomatic
a. Hematuria – if invades bladder
b. Rectal Bleeding – if invades bowel
F. PE
1. Dx w U/S
2. Vaginal/Manual exam contraindicated
3. Speculum exam to assess amount of bleeding
G. Management
1. Stabilize patient; Acute hemorrhage -> C/S
2. Hospitalize, FHR monitoring, 2 large bore IVs
3. Labs
a. CBC, T&C
Placenta Abruption
A.
B.
C.
D.
E.
Uterine Rupture
A.
B.
C.
b. If suspect coagulopathy -> DIC panel
c. If Rh negative -> RhoGAM dose
4. Prepare for catastrophic bleeding
5. Prepare for possible PTD (preterm)
a. MgSO4 and steroids
6. Consider amnio for FLM (fetal lung maturity) at 25-26 wk and C/S
delivery
General Considerations
1. Premature separation of a normally implanted placenta from the
uterine wall
Predisposing/Precipitating Factors
1. HTN (most common factor)
2. Prior abruption
3. AMA (advanced maternal age)
4. Multiparity
5. Uterine distention
6. Multiple pregnancy
7. Vascular deficiency
8. DM, Connective Tissue Disease
9. Cocaine/smoking
10. Trauma, etc…
Clinical Sx: 3rd trimester bleeding with severe abdominal pain and/or
frequent uterine contractions; may be asymptomatic
PE: bleeding, firm tender uterus, small frequent contractions, FHR often
non-reassuring d/t hypoxia
Management
1. Stabilize pt; deliver if hemorrhaging or non-reassuring FHR
2. Hospitalize, IV access, fetal monitoring
3. Labs: CBC & plts, T&C, PT/PTT, fibrinogen
4. If RH Negative, check KB & give RhoGAM
5. Prepare for possible hemorrhage
6. If stable, consider tocolysis and steroid Rx if < 34 wk
7. Vaginal delivery is preferred as long as bleeding is controlled and no
sign of abnormal FHR, labor is usually rapid
General Considerations
1. Most occur during course of labor
2. >90% associated w prior uterine scar
3. May develop hemorrhage and hypovolemic shock
Risk Factors
1. Prior uterine scarring
2. Injudicious use of Pitocin
3. Grand multiparity
4. Marked uterine distension
5. Abnormal fetal lie
6. Large fetus
7. External version
8. Trauma
Symptoms
1. Sudden onset of intense abdominal pain
2. +/- Vaginal bleeding
3. Non-reassuring FHR
Animal Bites General
Approach
Cat Bites
4. Disappearance of UCs on monitor
5. Regression of presenting part
D. Treatment
1. Immediate laparotomy and delivery of fetus
2. If feasible repair uterine ruptured site to obtain hemostasis
3. Discourage future pregnancies
4. No future TOL
5. Deliver future pregnancy by C/S consider amnio @ 36 wk for FLM
Bites/Stings (TEMM/Medicine Powerpoint)
• All bites should be considered tetanus prone.
• Consider injury potential for deeper structures and always get x-rays to
rule out underlying fractures and FB’s.
• All wounds require copious irrigation and necrotic tissue debridement.
Get those wound cultures first (aerobic and anaerobic).
• Given clinical presentation, always consider prophylactic antibiotics and
always establish close follow-up.
• Always remember to specify that your wound culture came from an
animal bite and specify the animal.
– Eikenella and Pasteurella are fastidious and are often misidentified.
– Always consider need for rabies prophylaxis. Any mammal can get
rabies!!
A. General Considerations
1. 5-18% of all reported animal bites
2. Most bites result in puncture wounds
3. 80% get infected – Pasteurella multocida is major pathogen
4. Rapid, intense, inflammatory response w/in hours of bite
5. Can lead to significant cellulitis, lymphangitis, septic arthritis, and
bacteremia
B. Treatment
-Adhere to standard wound care:
a. Trim any superficial devitalized epidermal tissue
b. Inspect the wound for evidence of deep puncture, especially near a
joint or scalp
c. Remove any foreign bodies or gross wound contaminants
d. Superficially irrigate the wound, AVOID HIGH PRESSURE
irrigation !!!
e. Consider soaking puncture wounds in an antiseptic solution
(e.g., betadine) x 15 min
-Do not suture puncture wounds or wounds < 1 to 2 cm.
-Do NOT use “skin glue” products to seal a wound.
-Augmentin is the drug of choice; other options include:
-Cefuroxime axetil (Ceftin) 500mg BID or Doxycycline 100mg BID
-DO NOT USE : Cephalexin (Keflex), Dicloxacillin or Clindamycin as
many strains of P. multocida are resistant to these antibiotics.
-Get a good wound culture (aerobic and anaerobic) prior to starting abx
(indicate source is animal bite)
-Update tetanus
-Consider coverage for possible Rabies exposure
-Est close follow up w/in 24-48 hrs
Dog Bites
A. General Considerations
1. 80-90% of animal bites
2. Adults – usually involve dominant hand
3. Children – usually on face or neck
4. Infection occurs in 5-15% of bites
5. Most bites are polymicrobial (alpha hemolytic strep, staph aureus,
pasturella, staph intermedius)
6. Dog bites more likely to involve full thickness and underlying tendon
and/or bony damage
B. Treatment
-Adhere to standard wound care:
a. Trim any superficial devitalized epidermal tissue
b. Inspect the wound for evidence of deep puncture, especially near a
joint or scalp
c. Remove any foreign bodies or gross wound contaminants
d. Superficially irrigate the wound, AVOID HIGH PRESSURE
irrigation !!!
e. Consider soaking puncture wounds in an antiseptic solution
(e.g., betadine) x 15 min, controversial for lacerated or larger
wounds (? delay in wound healing)
-Do not suture puncture wounds or wounds < 1 to 2 cm.
-Do NOT use “skin glue” products to seal a wound.
-Xrays
-Consider primary wound closure
-Clinically uninfected wounds
-<12 hrs old (24 hrs on face)
-Not located on hand or foot
-Rabies/Tetanus prophylaxis
-+/- Abx prophylaxis
-Augmentin 500mg TID (DOC)
-Clindamycin 300mg QID + FQ (if PCN allergic)
-Clindamycin + Bactrim (children)
-Wound care recheck and follow-up in 24-48 hours
Wasps, Bees, and
Stinging Ants
(Hymenoptera)
A. Clinical Features
1. Local Reactions: pain, erythema, edema, and pruritus at the sting site
a. Fire Ant Sting: sterile pustule that evolves over 6-24 hours
sometimes resulting in necrosis and scarring
2. Toxic Reactions
a. Non-antigenic result of a direct venom effect
b. Many similar features to allergic/systemic reaction but greater
frequency of GI disturbance while bronchospasm and urticarial are
infrequent
c. Symptoms typically subside w/in 48 hrs
d. Severe cases may last longer and lead to rhabdo and hepatorenal
failure
3. Systemic or Anaphylactic Reactions
a. Shorter interval btw sting and onset of symptoms = more severe
reaction
b. Nearly all episodes occur w/in 6 hrs; majority occur w/in 15 mins
c. Initial Symptoms: itchy eyes, urticarial, and cough
B.
Brown Recluse
Spider
A.
B.
C.
Black Widow Spider
A.
B.
d. As the reaction progresses -> respiratory failure, cardiovascular
collapse
4. Delayed Reactions:
a. 5-14 days after sting
b. Resemble serum sickness
c. Symptoms: fever, malaise, HA, urticarial, lymphadenopathy, and
polyarthritis
Emergency Department Care and Disposition
1. Remove the bee stinger and clean the wound w soap and water;
intermittent application of ice packs and elevation may reduce swelling
2. Local Reaction -> oral antihistamines and analgesics for symptomatic
relief
3. Anaphylaxis -> epi IM in thigh, repeat every 5 mins as needed
4. Hypotensive -> aggressive fluid resuscitation w normal saline 1-2L
5. Parenteral H1 and H2 blockers (diphenhydramine and ranitidine)
6. Sterooids to control persistent or delayed reaction
(methylprednisolone IV or prednisone PO)
7. Bronchospasm -> nebulized albuterol
Clinical Features
1. Initial bite is painless -> firm erythematous lesion -> necrotic w
significant eschars
2. Heals over several days to weeks
3. Patients with significant envenomation may exhibit hemolysis,
coagulopathy, or abnormal renal function
4. Loxoscelism – systemic reaction following the bite of some South
American species
a. Symptoms 1-3 days after envenomation – fever, chills, vomiting,
arthralgias, myalgias, petechiae, hemolysis …
Diagnosis and Differential
1. Violin–shaped pattern on cephalothorax of the brown recluse is
characteristic but unreliable
2. Diagnosis is commonly clinical; bites rarely witnessed
Emergency Department Care and Disposition
1. Supportive measures – pain medication, tetanus prophylaxis, abx if
infection present
2. Most wounds heal w/o intervention; role of dapsone in preventing
necrosis is controversial
3. Serial wound evaluation for outpatients
4. Patients w systemic reaction and hemolysis should be hospitalized
5. Sx reserved for lesions larger than 2 cm; deferred until 2-3 weeks after
bite
Clinical Features
1. Immediate pinprick sensation that quickly spreads to entire extremity
2. Erythema at site appears w/in 1 hr (target shaped lesion) along w
diffuse muscle cramps in large muscle groups (trunk, back, abdomen)
3. Severe pain may wax and wane for several days
4. Other S/Sx: HTN, tachycardia, HA, N/V, and diaphoresis
5. Serious Acute Complications: HTN, respiratory failure, shock, and coma
Emergency Department Care and Disposition
1. Local wound tx and supportive care (analgesics and benzos will relieve
pain and cramping)
Scorpion
A.
B.
Scabies
A.
B.
Ticks
A.
B.
C.
D.
2. Lacrodectus antivenom for severe envenomation
Clinical Features
1. Immediate pain and paresthesia
2. Positive “tap test” (exquisite local tenderness when the area is lightly
tapped)
3. Somatic and Autonomic Symptoms: tachycardia, N/V, excessive
secretions, roving eye movements, opisthotonos, fasciculations, cranial
nerve dysfunctions (vision and swallowing)
4. Symptoms may last 24-48 hrs w/o antivenom therapy
Emergency Dept Care and Disposition
1. Supportive tx: local wound care, analgesics, benzos
2. Atropine for hypersalivation and respiratory distress; contraindicated
for foreign scorpion stings
3. Severe systemic reaction -> antivenom
Clinical Features
1. Bites concentrated in web spaces btw fingers and toes; other common
areas include axilla and genital area, children’s faces and scalps, and
the female nipple
2. Transmission by direct contact
3. Distinctive Feature: intense pruritus w burrows; associated vesicles,
papules, crusts, and eczematization may obscure the dx
Emergency Department Care and Disposition
1. Permethrin cream – apply from neck down; bathe before application,
apply medication, bathe again in 12 hours; reapplication is only necessary
if mites are found 2 weeks after tx although pruritus may last for several
weeks after successful therapy
Lyme Disease
1. Caused by Borrelia burgdorferi
2. Prodromal symptoms include: fever, myalgias, arthralgieas, and HA
3. Erythema migrans: Macule or papule progressing to a plaque at site of
bite -> plaque expands and reddens -> central clearing leading to
annular or bull’s eye appearance
4. Stage I: constitutional symptoms and erythema migrans
5. Stage II – neuro (meningitis, encephalitis, bell’s palsy) or cardiac
complications (myocarditis, conduction blocks)
6. Stage III – consists of asymmetric, episodic, oligoarticular arthritis
7. Tx: Doxycycline or Tetracycline
Rocky Mountain Spotted Fever
1. Caused by Rickettsia rickettsia
2. Most cases occur btw April and October
3. S/Sx: fever, rigors, HA, myalgieas 7-10 days after inoculation
4. Characteristic Skin Rash (not always present): blanching macular
eruption on distal extremities -> palms and soles; becomes purpuric as
it spreads to the trunk and abdomen
5. Tx: Tetracycline or Chloramphenicol
6. Palmar and plantar petechiae in severely ill pt should be treated as
RMSF until proven otherwise
Tick Paralysis – symmetric ascending flaccid paralysis nearly identical to
Guillain-Barre
Erlichiosis, Babesiosis (malaria of northeast), Colorado Tick Fever,
Tickborne Encephalitis
Chiggers
Fleas
Lice
Bed Bugs
Pit Viper
E. Removal: grasp the tick w forceps near the point of attachment and pull w
steady, gentle traction
F. Disease transmission is time dependent; prompt tick removal is essential
A. Clinical Features
1. tiny mite larvae that cause intense pruritus when they feed on host
epidermal cells
2. attach to skin in areas of tight-fitting clothing such as near waistbands
3. Itchiness begins w/in a few hours followed by a papule that enlarges to
a nodule (chigger bite) over the next 1-2 days
4. Single bites may cause soft tissue edema whereas infestation has been
associated w fever and erythema multiforme
5. Dx based on typical skin lesions, intense pruritus, outdoor exposure
B. Emergency Department Care and Disposition
1. Tx is symptomatic w oral or topical antihistamines
2. Oral steroids may be required in more severe cases
3. Annihilation of the mites requires topical permethrin or other topical
scabicides
A. Frequently found in zig-zag lines, esp on legs and waist
B. Intensely pruritic w hemorrhagic puncta, surrounding erythema, and
urticarial
C. Discomfort is relieved w calamine lotion, cool soaks, and oral or topical
antihistamines
D. Severe irritation may require topical steroid creams
A. Body Lice
1. Concentrate on waist, shoulders, axillae, and neck
2. Bites produce red spots that progress to papules and wheals
3. Intensely pruritic, linear scratch marks are suggestive of infestation
4. Permethrin
B. Head Lice
1. White ova adhere to hair shaft (can distinguish from dander)
2. Treatment:
a. Application of pyrethrin w piperonyl butoxide after hair washing
b. Reapplication in 10 days
c. Wet combing hair w fine-tooth comb will remove dead lice and nits
d. Clothing, bedding, and personal articles should be washed in hot
water to prevent reinfestation
C. Pubic Lice
1. Spread by sexual contact
2. Intense pruritus; small white eggs (nits) visible on hair shaft
3. Treatment: same as for head lice
A. Feed on blood of sleeping victim
B. Initial bite is painless
C. Bites often linear; multiple, result in wheals or hemorrhagic papules and
bullae
D. Dark lines of bedbug excrement on bed linens may be seen
E. Tx: local wound care, topical steroids, oral antihistamines
A. General
1. Rattlesnakes, copperhead, water moccasin
2. Retractable fangs, heat sensitive depressions (pits) located bilaterally
B.
C.
D.
Coral Snake
A.
B.
C.
between each eye and nostril
3. Only 25% of bites result in envenomation
Clinical Features
1. Effects of envenomation depend on size and species of snake, age and
size of victim, time elapsed since bite, and characteristic of bite itself
2. Hallmark: presence of 1 or more fang marks combined w pain,
erythema, ecchymosis, and progressive edema extending form the site
3. Swelling usually occurs w/in 30 mins
4. Systemic Symptoms: N/V, weakness, perioral paresthesias, lethargy,
and weakness
5. More severe effects: tachycardia, tachypnea, respiratory distress,
altered sensorium, coagulopathy w elevated INR and prothrombin
time, hypofibrinogenemia, and thrombocytopenia
Diagnosis and Differential
1. Dx based on presence of the characteristic local injuries, systemic
symptoms, and hematologic abnormalities
2. Minimal envenomation – local swelling, no systemic signs, no lab
abnormalities
3. Severe envenomation – extensive swelling, potentially life-threatening
systemic signs and markedly abnormal coagulation parameters that
may result in hemorrhage
4. Lab Tests: CBC, coagulation tests, UA, blood typing
Emergency Department Care and Disposition
1. Consultation w poison control center
2. Properly placed constriction band (band wrapped circumferentially
proximal to the bite w only enough tension to gently impede venous
flow) may delay venous absorption
3. Cardiac monitoring and IV access
4. Local wound care & tetanus immunization
5. Measure wound circumference, check every 30 min while marking
border of advancing edema
6. Tx patients with progressive local swelling, systemic effects, or
coagulopathy immediately w antivenom therapy (FabAV)
7. Monitor blood count and coags every 4 hours
8. Look out for compartment syndrome – if it develops, elevate the limb,
give mannitol, additional FabAV; if pressures stay high, consider
fasciotomy
9. Observe for at least 8 hrs
10. Admit those w severe bites and those receiving antivenin to ICU
General
1. Coral: Red next to yellow, kill a fellow
2. Red next to black, venom lack
Clinical Features
1. S/Sx: tremor, salivation, respiratory paralysis, seizures, bulbar palsies
(dysarthria, diplopia, dysphagia)
Emergency Department
1. Consultation w poison control center
2. Toxic effects may be prevented, but not easily reversed
3. 3-5 vials of antivenin; additional doses if symptoms appear
4. Pulmonary function parameters and neuro exams
5. Admit to hospital for 24-48 hours of observation
General
Considerations
Clinical Features
A.
B.
C.
D.
E.
A.
B.
C.
Diagnosis and
Differentials
A.
B.
C.
D.
E.
Emergency
Department Care &
Disposition
A.
B.
C.
D.
Foreign Body Aspiration (TEMM)
Peak incidence between 1 & 3 years old
Most common
1. Food – peanuts, sunflower seeds, raisins, grapes, hot dogs
2. Toys
Suspect if hx of sudden onset of coughing or choking
Consider in all children w unilateral wheezing
Aspiration may be unwitnessed
May be asymptomatic
Primary Symptom: cough, classically abrupt in onset, may be associated w
gagging, choking, stridor, or cyanosis
Signs depend on location and degree of obstruction
1. Laryngotracheal obstruction – stridor, may have immediate onset of
severe stridor and cardiac arrest
2. Bronchial obstruction – wheezing; 80-90% of FBs are in the bronchus
Easily confused w more common causes of respiratory disease
1. Many patients have fever, wheezes, and rales
CXR
1. Can be normal (FB may be radiolucent)
2. Atelectasis may be present in case of complete obstruction
3. Hyperinflation of obstructed lung may be present w partial obstruction
d/t ball valve effect/air trapping
Laryngoscopy
1. FB aspiration is definitively dx preoperatively in only 1/3 of cases
2. If clinically suspected, laryngoscopy is indicated
Swallowed/Upper Esophageal FB
1. Usually radiopaque
2. Clinical Features: dysphagia, may have stridor if impinging on
posterior aspect of trachea
Esophagus v Trachea
1. Trachea - Flat FBs such as coins are usually oriented in the sagittal
plane (thick line on AP CXR)
2. Esophagus – Flat FBs such as coins are usually oriented in the coronal
plane (round on AP CXR)
If FB aspiration or airway obstruction is clearly present, perform BLS
procedures to relieve airway obstruction
If BLS maneuvers fail, undertake direct laryngoscopy w Magill forceps to
remove the FB. If the FB cannot be seen, orotracheal intubation w
dislodgement of the FB distally may be lifesaving
Consider racemic epi or Heliox as symptomatic palliatives
Definitive tx usually requires rigid bronchoscopy in the OR under general
anesthesia
Cardiac Failure/Arrest (AHA ACLS Manual)
ACLS Algorithm for
Cardiac Arrest
CPR Quality





Push hard (>/= 2 inches) and fast (>/= 100/min) and allow complete
chest recoil
Minimize interruptions in compressions
Avoid excessive ventilation
Rotate compressor every 2 mins
If no advanced airway, 30:2 compression-ventilation ratio


Return of
Spontaneous
Circulation (ROSC)
Shock Energy
Drug Therapy
Advanced Airway
Reversible Causes








•
•
•
•
•
•
•
•
•
•
•
•
•
Quantitative waveform capnography (If PETCO2 <10 mm Hg, attempt to
improve CPR quality)
Intra-arterial pressure (if relaxation phase (diastolic) pressure < 20 mm
Hg, attempt to improve CPR quality)
Pulse and blood pressure
Abrupt sustained inc in PETCO2 (typically >/= 40 mm Hg)
Spontaneous arterial pressure waves w intra-arterial monitoring
Biphasic: manufacturer recommendation (initial dose of 120-200 J); if
unknown, use maximum available. Second and subsequent doses should
be equivalent, and higher doses may be considered.
Monophasic: 360 J
Epinephrine IV/IO Dose: 1mg every 3-5 minutes
Vasopressin IV/IO Dose: 40 units can replace first or second dose of epi
Amiodarone IV/IO Dose:
- First dose: 300 mg bolus
- Second dose: 150 mg
Supraglottic advanced airway or endotracheal intubation
Waveform capnography to confirm and monitor ET tube placement
8-10 breaths per minute w continuous chest compressions
Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hypo/hyperkalemia
Hypothermia
Tension pneumothorax
Tamponade, cardiac
Toxins
Thrombosis, pulmonary
Thrombosis, coronary
Immediate PostCardiac Arrest Care
Algorithm
•
•
•
•
•
•
Ventilation/Oxygenation – avoid excessive ventilation. Start at 10-12
breaths/min and titrate to target PETCO2 of 35-40 mm Hg.
IV Bolus – 1-2L normal saline or LRs. If inducing hypothermia may use 4*C
fluid.
Epi IV Infusion – 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35
mcg/min)
Dopamine IV Infusion – 5-10 mcg/kg/min
Norepinephrine IV Infusion: 0.1-0.5 mcg/kg/min
Reversible Causes
Bradycardia w Pulse
Algorithm
Tachycardia w Pulse
Alg orithm
General
Fractures/Dislocations (PABR)
A. Definition
1. Break in the continuity of bone or cartilage
2. Pathologic fx occur through abnormal bone
3. Greenstick fx are incomplete angulated fx of long bones in children
B. Descriptors
1. Closed fracture: skin and soft tissue overlying the fx are intact
2. Open fracture: fracture exposed to the outside environment
*Give Cephalosporin (Ancef)
3. Types of fractures
a. Transverse
i. fx occurs at a right angle to the long axis of the bone
b. Oblique
i. fx runs oblique to the long axis of the bone
c. Spiral
i. fx encircles the shaft of the bone in a spiral fashion
d. Comminuted
i. fx where there are more than two fragments present
C. Epiphyseal Fractures
1. Salter-Harris Classification (SALT R)
a. Type I – fx extends through the epiphyseal plate, resulting in
displacement (same)
b. Type II – as above, plus triangular segment of metaphysis is
fractures (above)
c. Type III – fracture runs from the joint surface through
epiphyseal plate and epiphysis (lower)
D.
Ankle/Foot
A.
B.
C.
D.
E.
Forearm/Wrist/Han
d
A.
B.
d. Type IV – fracture as in type III but also through the adjacent
metaphysis (through)
e. Type V – crush injury of the epiphysis (rammed)
Accompanying Nerve Injuries
1. Certain nerve injuries may accompany certain fractures
a. Fx of Acetabulum – sciatic nerve
b. Fx of Femoral shaft – peroneal nerve
c. Fx of Humeral shaft – radial nerve
d. Fx of Lateral tibial plateau – peroneal nerve
e. Fx of Sacrum – cauda equina
Ankle fractures involve the lateral, medial, or posterior malleolus
1. MOI: eversion or lateral rotation on the talus
Foot fractures involve the talus, calcaneus, metatarsal, and phalanges
1. Talus fx d/t twisting injury, fall, or high-energy impact
2. Calcaneus fx d/t high-energy direct axial compression (look for fx of
spine as well)
3. Metatarsal fx d/t direct trauma or twisting force applied to a fixed
forefoot
4. Phalangeal fx d/t direct trauma, such as dropping a heavy obj or
stubbing toes
Deformity depends on extent of bone displacement
Diagnosis made by X-ray
1. Standard AP and lateral views plus AP view 15 degrees internally
rotated needed to dx ankle fx
2. Foot fx diagnosed by standard foot and ankle x-ray film
3. Ottawa Ankle Rules are used to determine if x-ray needed for foot or
ankle injuries
a. Ankle X-ray required if pain in malleolar zone and:
i.
Bone tenderness at posterior edge or tip of lateral malleolus
or
ii.
Bone tenderness at posterior edge or tip of medial malleolus
or
iii.
Inability to bear weight at time of injury and in ER
b. Foot X-ray required if pain in midfoot zone and:
i.
Bone tenderness base of 5th metatarsal or
ii.
Bone tenderness at navicular or
iii.
Inability to bear weight at time of injury and in ER
Treatment
a. Elevation and ice to control swelling
b. Casting w short leg cast
c. Referral is indicated w severe displacement
Boxer’s
1. MOI: direct blow of closed fist against another obj
2. Fx occurs at the distal end of the 5th metacarpal
3. Angulation of fx greater than 30* should be tx to limit deformity
4. Tx: splinting the jt in flexion or percutaneous pinning
Colle’s
1. MOI: fall on outstretched hand (FOOSH)
2. Transverse fracture of the distal radial metaphysis w dorsal
displacement of the distal fragment
a. Fx is located w/in 2 cm of the articular surface
C.
D.
E.
Hip
A.
B.
C.
b. Transverse fx of the distal radial metaphysis w volar displacement
of the distal fragment is reverse Colle’s or Smith fx
3. PE: “dinner fork” deformity of the wrist d/t dorsal displacement and
angulation of the fx
4. PA and lateral x-ray film of the wrist reveals a fx through the radial
metaphysis
5. Tx: fx reduction and sugar tong splinting w the wrist in flexion
Humeral
1. Humeral Shaft Fx
a. MOI: direct trauma or severe twisting of the arm
b. PE: localized pain w swelling; arm may be shortened or rotated
c. Complication: radial nerve injury
2. Supracondylar Fx
a. Fx of the distal humerus proximal to the epicondyles
b. Typically an injury of the immature skeleton and d/t fall on
outstretched hand (FOOSH) when elbow is fully extended or
hyperextended
c. Pts present holding the upper extremity in extension to the side w
swelling in the area of the elbow
3. Epicondyle Fx
a. Typically involves the medial epicondyle
b. MOI: repetitive valgus stress
4. Tx: simple immobilization w splint, cast, sugar tong, or sling and
swathe
a. If significant displacement is noted, a hanging cast may be required
Radial
1. MOI: FOOSH
2. PE: localized tenderness over the radial head or pain w passive
rotation of the forearm
3. X-ray: may be difficult to interpret; tenderness and + fat pad sign may
be only finding
4. Tx: sling support
Scaphoid
1. Most common carpal bone fx and most typically seen in young adults
2. MOI: FOOSH
3. PE: tenderness in anatomic snuffbox or w resisted supination; limited
ROM of wrist and thumb
4. X-ray: often negative
a. may require special scaphoid views or repeat x-ray 10-14 days after
tx
5. Tx: thumb spica and referral
a. Improper tx can lead to AVN
General
1. Incidence of hip fx doubles each decade of life after age 50
2. Women affected more often than men
3. Mortality rate is high
a. DVT and PE are serious complications
Clinical Manifestations
1. Pain is the major feature along w inability to bear weight
2. PE: affected leg is shortened and externally rotated
Diagnosis
D.
Knee
A.
B.
C.
D.
Shoulder
A.
B.
Dislocations
A.
1. X-ray film reveals fx
Treatment
1. sx repair, hip arthroplasty, is indicated
General
1. Result of significant trauma
a. Patellar fx d/t direct blow
b. Tibial plateau fx d/t impact, direct axial load, or shearing force
Clinical Manifestations
1. Presentation: knee pain and difficulty walking
2. PE: reveals swelling and bruising
3. Point tenderness over site of injury
Diagnosis
1. Patients present w large hemarthrosis w fat globules
2. X-ray film reveals fx
Treatment
1. Analgesics are required
2. The extremity should be immobilized and made nonweight-bearing
Clavicle
1. Very common fracture during childhood
2. MOI: direct force to lateral aspect of shoulder from a fall or sporting
injury
3. Presentation: pain over the fx site and the affected extremity is held
close to the body
4. Shoulder is typically slumped downward, forward, and inward
5. Typically heals w/o difficulty
a. If displaced may cause pressure on subclavian vessels or brachial
plexus
6. Tx is immobilization w figure eight dressing
7. Healing should be adequate in 6 weeks
Scapula
1. Uncommon fracture noted primarily in men 30-40 years of age
2. MOI: violent direct trauma
3. Typically no displacement
a. May have associated injury to ribs, chest wall, or shoulder girdle
4. PE: shoulder is adducted and the arm held close to the body
a. Inc pain w any movement
5. Tx: immobilization w a sling and swathe dressing
a. If significant displacement, the pt should be referred
Shoulder
1. Dislocation can be anterior or posterior
a. Anterior dislocation is most common
2. Mechanism of action
a. Anterior: d/t trauma from a fall or forceful throwing motion.
b. Posterior: posteriorly directed force when the arm is in adduction
and internal rotation
3. Clinical Manifestations
a. Sensation of shoulder slipping out of joint when arm is abducted
and externally rotated
i. Severe pain with movement of the shoulder
b. Anterior Dislocation – patient supports the arm in a neutral
position
i. Apprehension test positive in anterior dislocation
c. Posterior Dislocation – patient holds the arm in adduction and
internal rotation
i. Jerk test positive in posterior dislocation
d. Evaluate for possible axillary nerve injury
e. Abduction of the shoulder is impaired
4. Diagnosis
a. AP and Axillary shoulder x-ray films should be obtained
i.
X-ray reveals humeral head displaced inferiorly and
medially w an anterior dislocation
ii.
Compression fx of the posterior humeral head is evidence of
an anterior dislocation
iii.
Axillary view needed to dx posterior dislocation
b. MRI or Arthrogram may be needed for dx
5. Treatment
a. Dislocation should be reduced and physical therapy begun to
strengthen the rotator cuff muscles
b. Sx may be needed to correct recurrent dislocations
B. Elbow
1. General
a. Elbow dislocation results from FOOSH w elbow extended
b. Most are posterior and can be complete or perched
c. Concomitant fractures, of the radial head in adults or medial
epicondyle in children, are common
2. Clinical Manifestations
a. Present w severe pain, swelling, and inability to bend elbow
b. Must evaluate brachial artery, median nerve, and ulnar nerve for
injury
i.
Weakness with wrist flexion and finger adduction with
median nerve injury
ii.
Weakness w finger abduction with ulnar nerve injury
3. Diagnosis
a. AP and lateral x-ray film assist in the dx
4. Treatment
a. Reduction of the elbow should be performed as soon as possible
i. Hold elbow flexed at 45* and apply slow, steady, downward
traction on the forearm
b. After reduction the arm should be splinted
5. Nursemaid’s Elbow (subluxation of radial head)
a. Common elbow injury in children younger than 5 d/t dec ligament
laxity
b. MOI: pull on forearm when elbow is extended and forearm
pronated
c. Clinical Manifestations: pain, child reluctant to use arm, extremity
held by side with elbow slightly flexed and forearm pronated,
tenderness over radial head
d. Diagnosis: x-ray film is normal; based on clinical findings
e. Treatment: reduction (place thumb over the radial head and
supinate the forearm)
C. Hand
1. General
a. Common injury d/t hyperextension injury
a. Involves complete tear of volar capsule
b. PIP jt is most commonly affected
2. Clinical Manifestations
a. Note jt deformity immediately after the injury
b. Joint instability is also noted
3. Diagnosis
a. Xray films are needed to r/o fx
4. Treatment
a. Closed reduction is required for PIP and DIP jt dislocations
b. Buddy taping to adjacent finger will stabilize joint
D. Hip
1. General
a. Occur when femoral head is displaced from the acetabulum
b. Typically occur d/t high energy trauma, such as an MVA
c. Two Types
i.
Posterior – most common
ii.
Anterior
2. Clinical Manifestations
a. Posterior
i.
His is short and fixed in flexion, adduction, and internal
rotation
ii.
Sciatic nerve injuries are common
b. Anterior
i.
Hip is in mild flexion, abduction, and external rotation
position
ii.
Femoral artery and obturator nerve injury may be present
3. Diagnosis
a. Xray film of posterior dislocation reveals the affected femoral head
appearing smaller than the opposite side
b. Xray film of an anterior dislocation reveals affected femoral head
appearing larger than the opposite side
4. Treatment
a. AVN can occur d/t vascular compromise
i. More common in posterior dislocation
b. Reduction should occur as soon as possible, after a fx has been r/o
c. After reduction, crutch-assisted ambulation w limited weight
bearing until pain free
E. Knee
1. General
a. Severe injury resulting from violent trauma
b. Typically have three to four major ligaments injured w dislocation
c. Vascular and nerve injuries are common
d. Classification based on direction of dislocation: anterior, posterior,
lateral, medial, and rotatory
i.
Anterior dislocation is d/t hyperextension of the knee
ii.
Posterior dislocation is d/t direct blow to the anterior tibia
w knee flexed 90*
e. Patella dislocation is d/t twisting injury on an extended knee
i. More common in females
2. Clinical Manifestations
Fingers
a. Obvious deformity may be noted
1. Dimple sign on the anteromedial surface is noted in
posterolateral dislocation
b. N/V complications are common and status must be evaluated in all
patients
1. Complications involve popliteal artery and peroneal nerve
c. Patella dislocation presents w patella displaced laterally over the
lateral condyle
3. Diagnosis
a. X-ray film is required to determine the direction of the dislocation
and presence of any fx
4. Treatment
a. Reduction should be undertaken immediately
i. After reduction, the knee should be immobilized
b. If reduction is not possible or vascular injury is present, immediate
surgical intervention is required
c. Flexing the hip, hyperextending the knee, and sliding the patella
back into place reduce patella dislocation
i. Immediate pain relief
F. Ankle/Foot
1. General
a. Can occur in one of four planes and are commonly associated w a
fracture
b. Posterior dislocation occurs when a backward force is applied
when the foot is plantar flexed
c. Anterior dislocation occurs when force applied to anterior aspect of
the tibia w the foot dorsiflexed
2. Clinical Manifestations
a. Pain, swelling, and deformity at site of injury
b. Patient is unable to bear weight and ROM is dec
c. N/V compromise can occur; peroneal nerve is at risk
3. Diagnosis
a. Xray film reveals widening of joint spaces
4. Treatment
a. All dislocations of the ankle should be referred
b. Closed reduction should be performed immediately to limit risk of
ischemia
i. Open reduction and fixation and posterior splint are typically
required
Sprains/Strains (PABR)
A. General
1. Typically a result of either radial or ulnar collateral ligament injury to
the PIP or DIP joints
2. Etiologies: sports, falls, work-related trauma, or direct blows
3. Grades
a. Grade 1 – damage to the ligament but no joint instability
b. Grade 2 – stretching and partial tearing of the ligament
c. Grade 3 – complete disruption of the ligament
B. Clinical Manifestations
1. Grade 1 – swelling and tenderness to palpation, but no functional
abnormality
C.
D.
Back
A.
B.
C.
D.
Knee
A.
B.
2. Grade 2 – swelling with bruising is noted with some joint laxity
3. Grade 3 – joint is painful and feels unstable
Diagnosis – based on clinical findings
Treatment
1. Grades 1 & 2 tx w buddy taping injured finger to adjacent finger
2. Grade 3 – buddy tape, refer for sx
General
1. D/t injury to the paravertebral spinal muscles, ligamentous injuries of
the facet joints, or annulus fibrosis
a. Sprain – damage to ligaments
b. Strain – damage to muscles
2. Precipitated by repeated lifting and twisting
3. Risk factors include poor fitness, smoking, and hypochondriasis
Clinical Manifestations
1. Symptoms are typically of limited duration
2. Pain radiates into the buttocks and posterior thigh
3. Patient may have trouble standing erect
4. Physical examination reveals diffuse tenderness in the lower back or SI
region
5. ROM is dec, esp flexion
6. Sensory exam and DTRs are normal
Diagnosis
1. X-rays only needed if atypical symptoms present
a. Includes pain at rest, pain at night, or significant trauma
Treatment
1. Cold therapy is started first followed by heat therapy after 48-72 hours
2. Pain medications with NSAIDs or other non-narcotics
3. Muscle relaxants may be helpful first 3-5 days
4. After pain has resolved, strengthening and conditioning should be
started
Medial Collateral Ligament Injury
1. General
a. Mechanism of injury is direct blow to the lateral portion of the knee
(valgus)
2. Clinical Manifestations
a. Patients report hearing or feeling a pop over the medial knee
b. Medial knee pain and swelling
c. Ligament is tender to palpation
d. Degree of injury is evaluated by applying valgus stress to the knee
when full extended and in 20-30* of flexion
3. Diagnosis
a. Based on H&P
4. Treatment
a. Conservative therapy with RICE
b. Bracing may be helpful
Lateral Collateral Ligament Injury
1. General
a. MOI: direct blow to the medial knee or anteromedial tibia w the knee
flexed and foot planted
2. Clinical Manifestations
a. Pain, stiffness, and localized swelling
Ankle/Foot
b. Varus stressing of the knee reveals inc laxity
c. If peroneal nerve damage is present, weakness of foot dorsiflexion
and eversion is noted
3. Diagnosis
a. Based on H&P
4. Treatment
a. Surgical repair is indicated
C. Anterior Cruciate Ligament Injury
1. General
a. MOI: direct blow or indirect stress; requires sudden change in
direction of the weight-bearing knee
2. Clinical Manifestations
a. Immediate swelling and pain after injury
b. Knee is very unstable and weight bearing is difficult
c. Pain and tenderness is noted in the posterolateral area of the knee
or near the tibial plateau
d. Positive anterior drawer or Lachman test
3. Diagnosis
a. Based on H&P
4. Treatment
a. Referral is needed for possible surgery
D. Posterior Cruciate Ligament Injury
1. General
a. MOI: hyperextending the knee or a direct blow to the anterior
proximal tibia w the knee flexed and foot planted
2. Clinical Manifestations
a. Dull aching pain and stiffness; swelling is not typical
b. PE: mild effusion and posterior drawer test positive
3. Diagnosis
a. Based on H&P
b. MRI may be used to evaluate for possible ligament damage
4. Treatment
a. Conservative tx and physical therapy may be successful
b. Surgical intervention is the tx of choice
A. General
1. Injury to the lateral ligaments is most common
a. Injury to the syndesmosis (anterior tibiofibular ligament) is less
common and called a high ankle sprain
2. MOI: increased rotational stress
a. Inversion injury is most common for lateral ankle sprain
b. Eversion injury leads to medial ankle sprain (deltoid ligament)
c. Forceful external rotations lead to syndesmosis injury
3. Grading of Injury
a. Grade I
i.
Ligaments stretched but no tear
ii.
Ankle painful, but stable and has normal function
b. Grade II
i.
Some ligament tearing with moderate swelling and pain
ii.
Some function limitations
c. Grade III
i. Complete tear of the ligament with marked swelling, bruising, and
General
A.
B.
Risk Factors for
Coronary Artery
Atherosclerosis
A.
B.
C.
D.
E.
F.
G.
H.
I.
J.
A.
Clinical
Manifestations
B.
C.
D.
E.
joint instability
B. Clinical Manifestations
1. Pain, swelling, and loss of function are common
2. PE: noted ecchymosis and swelling around entire ankle
3. Injury to the syndesmosis is noted by a positive squeeze test and
external rotation test
4. Lateral ankle sprain will have a positive anterior drawer test and talar
tilt test
a. Anterior drawer evaluates the anterior talofibular ligament
b. Talar tilt test evaluates the calcaneofibular ligament
C. Diagnosis
1. AP, lateral, and mortise views requires to r/o fx
D. Treatment
1. Initial tx is NSAIDs and RICE
2. Brace to provide support and promote soft-tissue healing
Myocardial Infarction (PABR)
Myocardial necrosis brought on by ischemia
Most deaths occur w/in 1 hr of onset of symptoms
1. Most deaths caused by VFib
2. Rapid defibrillation can reverse VFib
Hyperlipidemia
HTN
Increasing age
Obesity
Positive Fam Hx
Stress
DM
Male Gender
Sedentary Lifestyle
Smoking
Pain is restrosternal and described as heavy, pressure-like, squeezing, or
bandlike
1. pain may radiate to neck, jaw, or left arm
2. Pain typically lasts longer, 20 mins to several hrs, than angina
3. Elderly pts or pts w DM may have acute MI that is painless
4. Watch for atypical presentation of pain
Associated symptoms include N/V, diaphoresis, dyspnea, and weakness
Physical Exam reveals no findings that are diagnostic for acute MI
1. BP may be elevated, S4 may be noted, Signs of heart failure may be evident
Lab Studies
1. Myoglobin – detectable 1-2 hrs after AMI, found in skeletal and cardiac mm.
2. CPK – Total CPK correlated w infarct size, CPK-MB is specific for cardiac
muscle
3. Troponin – not normally present in blood; elevated in AMI
a. Troponin I is test of choice
4. Other Tests
a. Leukocytosis noted on CBC
b. C-reactive protein is elevated
EKG
a. may reveal ST elevation
Diagnosis
Treatment
Complications
Essentials of
Diagnosis
A. Based on clinical and lab findings
B. Echocardiogram is obtained to evaluate global and regional cardiac function
C. Coronary angiography confirms location of injury and coronary vessel
involved
A. ASA should be given to all pts unless contraindicated
B. Initial Therapy
1. Oxygen – given to avoid hypoxia
2. Beta-Blockers – control BP and dec probability of sudden cardiac death
3. Nitroglycerin – used for coronary artery dilation
4. Morphine – pain and BP control
5. Continuous EKG monitoring
C. Specific Therapy
1. Thrombolytic Therapy (streptokinase and tissue plasminogen activator)
a. Major risk factor is bleeding, intracerebral hemorrhage
b. Candidates for therapy include pts w ST elevation or new LBBB
presenting w/in 12 hrs of onset of symptoms w/o contraindications
2. Primary Percutaneous Coronary Intervention
a. Mechanical recanalization by inflation of catheter-based balloon
b. Preferred over thrombolytics
3. Antiplatelet
a. ASA – inhibits platelet aggregation and development of coronary
thrombi
b. Clopidogrel – antiplatelet effects and used in asa-allergic pts
c. Glycoprotein IIb/IIIa inhibitory (Abciximab or Eptifibatide) – inhibits
fibrinogen receptor and benefits high-risk patients by improving
coronary artery patency
4. Antithrombin – heparin inactivated thrombin and factor X; used in
combination w thrombolytic therapy
5. Other
a. Nitrates – induce vascular smooth muscle relaxation and reduce cardiac
preload and afterload
b. Beta-blockers – reduce HR, BP, and myocardial contractility, and
stabilize the heart electrically
i. Limit myocardial oxygen consumption
c. ACEi – improves remodeling after AMI, avoid in presence of
hypotension
A. Arrhythmias
1. Ventricular
2. AFib
B. Heart Failure
1. LV dysfunction
2. Cardiogenic shock
C. Mechanical
1. Papillary muscle rupture
2. LV wall rupture
3. LV aneurysm
D. Thromboembolic
Hypertensive Crisis (PABR)
A. Hypertensive Crisis is typically defined as systolic BP >220 mm Hg or
diastolic BP > 125 mm Hg
General
Considerations
Demographics
Symptoms & Signs
Diagnosis
Treatment
Follow-up
B. Development of acute end organ damage depends on:
1. Rate of rise in BP
2. Magnitude of inc in BP
3. Presence of underlying conditions
A. Hypertensive Urgency – systolic BP > 220 mm Hg or diastolic BP > 125
mm Hg w/o evidence of acute end-organ damage
B. Hypertensive Emergency – acute hypertensive injury to heart, brain,
retina, kidneys, aorta, and/or eclampsia
C. Malignant HTN – typically occurs in context of renal dz; characterized by
hemolysis and platelet consumption d/t fibrinoid necrosis in arterioles
A. Usually occurs in people w preexisting HTN
B. Often d/t abrupt cessation of antihypertensive therapy
C. Also occurs in setting of acute renal failure or use of high doses of
sympathomimetics
Depend on organ involved
A. HA, irritability, confusion, and somnolence are signs of encephalopathy
B. Chest pain or dyspnea occurs w cardiopulmonary involvement
C. Back pain occurs w aortic dissection
D. Blurry or diminished vision occurs w retinal involvement
E. Cardiac exam may reveal low A2, an S4, or a murmur of aortic
regurgitation
F. Papilledema is indicative of elevated intracranial pressure
G. Crackles on lung exam occur w CHF
A. Lab Tests
1. CBC (platelet consumption…)
2. UA
3. Serum Creatinine, BUN, Troponin, Creatine Kinase
4. EKG
5. CXR
6. Consider urine screen for cocaine
B. Diagnostic Procedures
1. CNS Symptoms -> Head CT to r/o bleed/infarct
2. Chest Pain -> EKG to r/o ACS; CXR to r/o thoracic aortic dissection
3. Renal Dysfunction -> Renal US to r/o obstruction or CKD
A. Hypertensive Urgency
1. Goal – relieve symptoms/bring BP to reasonable level w/in 24-48 hrs
2. Clonidine, captopril, metoprolol, and hydralazine are effective oral
agents
3. Avoid B-blockers if cocaine use; Avoid ACEi if renal artery stenosis
suspected
B. Hypertensive Emergency
1. Goal – reduce MAP by 25% in 1-2 hr; then reduce BP to 160/100 mm
Hg over next 6-12 hrs
2. If Ischemic Stroke, only tx if systolic BP exceeds 180/200 mm Hg
3. Avoid excessive reduction bc it can lead to coronary, cerebral, or renal
hypoperfusion
4. In most situations, appropriate BP control is best achieved by using
combinations of nicardipine or clevidipine, labetolol and esmolol
5. Nitroprusside, labetalol, and nitroglycerin are most commonly used IV
Follow up in 48-72 hours to ensure adequate BP control, tolerability and
Complications
When to Admit
General
Risk Factors
Pathophysiology
Clinical
Manifestations
Diagnosis
compliance of regimen
A. Stroke
B. MI
C. CHF
D. Retinal vasculopathy
E. Aortic dissection
F. Acute kidney injury
A. Hypertensive Urgency – hospitalization rarely needed
B. Hypertensive Emergency – all patients, in particular patients with the
following (usually ICU admission) /
1. Encephalopathy
2. Neuro deficits
3. Chest pain
4. Dyspnea
5. Papilledema
6. Hematuria
7. Renal dysfunction
8. EKG changes
9. Eclampsia
Pulmonary Embolus (PABR)
 Most PE arise from venous thrombi in deep veins of lower extremities
followed by right-sided heart chamber, pelvic veins, and venous catheters
 Emboli are usually multiple and bilateral and typically found in the lower
lobes
 Hypercoagulable states
 Pregnancy and BCP
 Recent orthopedic, neuro, or gynecologic sx w general anesthesia
 Recent major trauma
 Afib
 Right ventricular MI
 Immobilization
 Hx of prior PE
Total stoppage of blood flow to the distal lung leads to respiratory and
hemodynamic changes
A. Respiratory Changes
1. Area of lung is ventilated but not perfused
2. Pneumoconstriction -> stoppage of pulmonary capillary flow
3. Loss of surfactant -> alveolar collapse
B. Hemodynamic Changes
1. Inc resistance to blood flow through the lung -> acute right ventricular
strain, dec cardiac output, inc in HR
A. Must have high index of suspicion
B. Sx: acute onset of dyspnea, pleuritic chest pain, cough, hemoptysis,
syncope, and substernal chest pain
C. Physical Exam: tachycardia & tachypnea
1. Most pts lung exam is normal
2. In a massive PE, an S3 may be noted
A. ABG – acute respiratory alkalosis
B. EKG – S1Q3T3 w or w/o right bundle branch block
C. CXR – most abnormalities non-specific
D.
E.
F.
G.
Treatment
A.
B.
C.
D.
General
A.
B.
C.
D.
Primary
Spontaneous
A.
Secondary
Spontaneous
Traumatic
Tension
B.
C.
D.
A.
B.
C.
A.
B.
A.
B.
C.
1. Westermark’s Sign – area of dec pulmonary vascularity with a cutoff
sign
2. Hampton’s Hump – shadow or density in contact w one or more
pleural space corresponding to lung segment involved
Elevated D-Dimer – excellent for ruling out PE in low probability pts
V/Q Scan
1. Scored: Normal, Low, Intermediate, or High Probability
2. Use limited if other lung pathology is present
3. Replaced by spiral CT, used if pt is pregnant
Spiral CT Scan
Pulmonary Angiography
1. Gold standard
2. Very invasive w inc morbidity and mortality
Prevention
1. Early ambulation after sx or delivery, heparin therapy for high-risk pts,
or compression stockings
Anticoagulation
1. Heparin is gold standard for acute therapy
a. LMWH can be used– less bleeding likely, no lab monitoring needed
2. Long-term therapy includes warfarin/coumadin
Pulmonary Embolectomy
1. Rarely needed except for large saddle emboli
Vena Cava Filter
1. Indications include absolute contraindication to anticoagulation,
recurrence of PE or bleeding while on anticoagulation, or septic emboli
from a pelvic source
Pneumothorax (PABR)
D/t presence of air in the pleural space
Clinical Manifestations: sudden onset of dyspnea and pleuritic chest pain
Physical Exam: dec or absent breath sounds
CXR: essential to confirm dx; reveals a collapsed lung w loss of lung
markings at the periphery
Occur in absence of underlying lung dz
1. Seen most commonly in thin males aged 20-40 yrs
Typically d/t rupture of pleural blebs and occur almost exclusively in
smokers
Recurrence is common
Tx is simple aspiration or pleural abrasion to prevent recurrences
Occurs in the presence of underlying lung disease such as COPD
More life threatening
Tx: chest tube, use of sclerosing agent
Results from penetrating or non-penetrating chest injuries
Tx: chest tube unless pneumothorax is very small
Pneumothorax in which the pressure in the pleural space is positive
throughout the respiratory cycle
1. Occurs most commonly during mechanical ventilation or pulmonary
resuscitation
Life threatening d/t positive pressure in thorax dec venous return and
cardiac output
Physical Exam: dec or absent breath sounds on affected side, shift of
Initial Approach
mediastinum to contralateral side
D. CXR – collapsed lung w mediastinal and tracheal shift away from the
pneumothorax; should be clinical dx
E. Tx: rapid placement of large-bore needle into pleural space through the
second anterior intercostal space
Ingesting Harmful Substances/Poisonings (Medicine Powerpoint)
A - Airway Assessment
B – support ventilation if needed
C – Circulatory assessment and support
C – “coma cocktail” (Narcan, thiamine, D50)
Hx – often lacking, key historians often not the pt, helpful to know ALL Rx meds in
the house, review old records
PE – identify signs of toxidromes
Tox Work-Up










GI Decontamination




Opioid Toxidrome
Urine Drug Screen – most ordered test on Tox patients, most worthless,
drugs that appear are rarely the drugs in the acute OD
Serum Alcohol Level – can be useful if pt is acting funny (esp in peds) and
for medio-legal aspects
Urinalysis – crystals, rhabdomyolysis, pregnancy
CXR – as a rule…worthless, unless you suspect pulmonary edema or
aspiration
KUB – mostly worthless, can see heavy metal ingestion (iron, lithium, MVI,
etc.)
Specific Drug Levels – based on both ingestion hx and available meds in
the house; order ASA and Tylenol drug levels in every pt
Total CPK – rhabdomyolysis
EKG – good positive predictive value; widened QRS, prolonged QT,
“scooped” ST segments
ABG – useful with certain ingestions, routine ordering not useful
BMP – Na, K, Cl, BUN, Cr, Ca, Glucose, HCO3; order on ALL possible
ingestions
 Anion Gap Acidosis – never ignore
 Anion Gap = (Na + K) – (Cl + HCO3) = 10-12 normally
 MUDPILES – methanol, uremia, DKA< paraldehyde,
INH or Iron, Lactic acidosis, ethylene glycol,
salicylates
Activated Charcoal (AC) – high affinity for ASA and anticonvulsants, does
not bind heavy metals or alcohols, typical dose 1g/kg (50g PO)
Gastric Lavage – “stomach pump”, rarely used unless truly toxic ingestion
(ie no antidote – antihypertensives?) who presents w/in 1 hour, elective
intubation prior to lavage is standard practice
Whole Bowel Irrigation (WBI) – NG or OG tube instillation of PEG lavage
fluid in serial fashion; rarely used unless toxic drug poorly bound by AC or
certain sustained release preps, also for “body packers”
Dialysis – invasive and expensive, used for toxic alcohols, ASA, and heavy
metals
A. Agent: opiates, sedatives, hypnotics, alcohol in high doses
B. S/Sx: coma, respiratory depression, miosis (pinpoint), hypotension,
C.
Sympathomimetic
Toxidrome
Anticholinergic
Toxidrome
A.
B.
C.
A.
B.
C.
Cholinergic
Toxidrome
A.
B.
C.
Acetaminophen
Toxicity




Ethylene Glycol




bradycardia, hypothermia, pulmonary edema, dec bowel sounds,
hyporeflexia, needle makrs
Tx: ABCs, Narcan (2mg IV bolus for true bradypnea; 0.25mg IV for mild to
moderate sx)
Agent: cocaine, meth, etc.
S/Ss: paranoid, tachycardic, HTN, hyperpyrexia, diaphoresis, mydriasis
(dilated), piloerection
Tx: ABCs, Benzos (Ativan 1-2mg IV as needed)
Agent: jimson weed, Benadryl, scopolamine, Dramamine, belladonna,
thorazine
S/Sx: mad as a hatter (delirium), dry as a bone (dry skin/urinary
retention) red as a beet (flushed skin), hot as hell (elevated temp), blind as
a bat (visual changes; mydriasis w loss of accommodation)
Tx: mainly supportive (early intubation?), Benzos for agitation, standard
ACLS drugs for dysrhythmias, watch fro rhabdomyolysis, BEWARE
Physostigmine
Agent: organophosphates, pesticides, mushrooms, etc.
S/Sx: SLUDGE (salivation, lacrimation, urination, defecation, GI cramps,
emesis)
Tx: early intubation for severe poisonings (succinylcholine lasts longer),
decontamination, Atropine 2-5 mg every 5 minutes or 2-PAM
(pralidoxime) 2 gm bolus followed by 1gm/hr infusion
Most absorption w/in 2 hrs, peak levels w/in 4 hrs, toxic dose 140 mg/kg
Mechanism of toxicity – acetaminophen metabolized to NAPQI a toxic
metabolite, NAPQI + GSH = non-toxic conjugate; when NAPQI exceeds GSH
then NAPQI exerts its hepatic toxicity
Four Stages of Clinical Symptoms:
o Pre-Injury: minimal sx w/in first 24 hours (nausea, anorexia, etc)
o Onset of Liver Injury: RUQ pain, vomiting, usually occurs after 24 hours
o Maximal Liver Injury: fulminate hepatic failure, usually 3-4 days
o Recovery: hepatic enzymes return to normal w/in 5-7 days
Acute Ingestion:
o Toxic level of acetaminophen >140 at 4 hours
o Tx: N-Acetylcysteine (NAC) for toxic levels
 NAC – GSH substitute and precursor
 8 hour time window
 140 mg/kg of NAC (IV – for intractable vomiting,
pregnancy, or hepatic failure)
 17 doses at 4 hour intervals
o AST is screening tool for hepatic injury
Workup: UA (fluorescent crystals), ECG, BMP, Serum Osmolarity, ASA and
Acetaminophen Levels, EtOH level
Osmol Gap + Anion Gap = Double Gap acidosis = TRUE emergency
 Calculated Osmolality = (2x (Na+K)) + (BUN/2.8) +
(glucose/18); Measured – Calculated = Gap; OG > 10 =
critical
Mechanism: Ethylene Glycol produces toxic metabolites -> severe
metabolic acidosis
S/S: pt appears intoxicated w/o the smell of EtOH, Double Gap Acidosis

Caustic Ingestions






ASA Overdose




General
Clinical
Manifestations
A.
B.
C.
A.
B.
C.
Diagnosis
Treatment
D.
A.
A.
B.
(sick, sick, sick), Ca+ Oxalate crystals in urine (fluorescence with Wood’s
Lamp)
Management: aggressive Bicarb, ethanol or 4MP (Class C) used to block
ADH, hemodialysis is cornerstone (indications controversial)
Alkali > Acid (liquefaction v coagulation necrosis)
Caustic burns graded as partial or full thickness (just like thermal)
PE: look for oral burns (positive predictive value is poor but negative
predictive value is good), dysphagia and drooling
Management: laryngeal edema can occur over minutes to rapid intubation
may be needed (be ready for surgical cricothyrotomy, BNTI – blind
intubation contraindicated)
Dx Tests: CXR (useful to dx mediastinal or abd free air); Endoscopy
(indicated for sx patients and presence of oral burns; late endoscopy
hazardous secondary to wound softening)
Tx: gentle oral fluids or milk in small amounts for dilution, emesis and AC
have NO role, steroids (controversial), no abx
Toxic Dose = 250mg/kg; Lethal Dose = 500mg/kg; peak levels in 2-4 hours
Toxic Effects: stimulates respiratory center -> hyperventilation ->
respiratory alkalosis; uncouples oxidative phosphorylation -> inc
metabolic rate -> metabolic acidosis; renal failure and hypokalemia,
pulmonary edema and cerebral edema, tinnitus and hyperthermia
Dx Tests: 4-6 hour ASA level, if initial level undetectable -> nontoxic
ingestion; if initial level is in nontoxic range -> repeat in 2 hours
Management: prevent further absorption, correct acid-base, inc excretion
 MDAC (activated charcoal), consider WBI for large enteric
coated ASA ingestions
 Aggressive IV fluid hydration
 Frequent accu-checks
 Repleat K+
 Urine alkalinization (bolus followed by drip) for ASA > 35
 Dialysis for ASA > 100, severe acidosis, rising levels, or other
“serious” signs
Orbital Cellulitis (PABR)
Occurs most commonly in children
May be the result of trauma or extension of sinusitis through the ethmoid
sinus to the orbit
Most common organisms are H. influenza and S. pneumonia
Children may present w proptosis
Symptoms: edema, erythema, hyperemia, and pain
1. Infection may spread rapidly
Physical Examination: chemosis, limited eye movements, reduction of
vision, and erythema
1. Limited eye movements noted in post-septal cellulitis
Labs: leukocytosis
CT scan or MRI needed to separate preseptal from postseptal involvement
Nasal decongestants and vasoconstrictors may help to drain sinuses
IV abx are required
1. Mild cases tx w amoxicillin and severe cases tx w ceftriaxone and
vanocmycin
*Sources: Tintinalli’s Emergency Medicine Manual (TEMM), Physician Assistant Board Review 2nd Edition
(PABR), AHA ACLS Manual, Medicine Powerpoints