29

USMLE Step 3 (Subject) / Emergency Medicine (Lesson)

This lesson was created by estoffel.

Learn lesson

back  |  next 1 / 1

• The 2° survey The 2° survey consists of total patient evaluation. This is also the time to order appropriate lab tests and radiographs based on the mechanism of injury, past medical history, and the like. - Obtain an AMPLE history: Inquire about Allergies, Medications, Past medical history, Last oral intake, Events/Environmental factors related to the injury. If the patient can speak, ask about other symptoms that may not be obvious on exam. Obtain as much information as possible from EMTs/paramedics about the circumstances of the trauma.- Conduct a focused physical exam:→ Head and skull: Inspect for trauma, pupils, and loss of consciousness. Look for ecchymosis around the eyes ("raccoon eyes") and hemotympanum, which point to a basilar skull fracture. Inspect the ears and nose for CSF leakage. If a septal hematoma is present, it will need to be drained once the patient is stabilized. Assess for midface instability, ocular/orbital trauma, or intraoral injuries. Ecchymosis of the mastoid process (Battle's sign) is a late sign of basilar skull fracture and is rarely found on initial presentation.→ Neck: Look for trauma or a pulsatile/expanding hematoma; palpate for midline tenderness, crepitus, and tracheal deformity.→ Chest: Inspect for irregular or paradoxical breathing patterns resulting from multiple rib fractures – i.e., flail chest. Listen for equal and bilateral breath sounds (If absent/asymmetric or if there is crepitus on palpation of the chest, suspect pneumothorax; however, be aware that absent breath sounds are only 80% sensitive). Listen for clear heart sounds (if muffled and accompanied by JVD, suspect cardiac tamponade). A new diastolic murmur after trauma suggests aortic dissection.→ Abdomen: Inspect the abdomen and flanks for signs of trauma. Palpate the pelvis for tenderness or instability. Do not compress the pelvis anteriorly/posteriorly; if the patient has an "open book" fracture, doing so will make it significantly worse.→ Perineum/rectum/vagina: Assess for trauma, including urethral bleeding (suggests urethral tear). Check for prostate position, rectal tone, and rectal blood. Check women for vaginal trauma and blood in the vaingal vault.→ Musculoskeletal system: Look for evidence of trauma, including contusions, lacerations, and deformities. Inspect the extremities for tenderness, creptius, abnormal range of motion, and sensation. An externally rotated, shortened leg suggests hip fracture.- Imaging:→ Head and skull: Obtain a CT of the head and face if there is evidence of trauma. Maintain a low threshold for scanning intoxicated patients, elderly patients, and those on blood thinners.→ Neck: Maintain in-line immobilization and protection with hard cervial collar. Obtain radiographs if the cervical spine cannot be cleared clinically. If indeterminate, consider CT of the cervical spine.→ Chest: Rapidly assess for pneumothorax with ultrasound. Obtain a CXR in all patients with significant trauma. Penetrating thoracic wounds or clinical concern for major intrathoracic trauma often requires a chest CT.→ Abdomen: Obtain a pelvic x-ray; arrange for a FAST scan and/or an abdominal CT if indicated. Diagnostic peritoneal lavage is rarely done anymore.→ Urinary system: If there is blood at the urethral meatus or a "high-riding" prostate, consult urology for a urethrogram. Do not insert a Foley.→ Musculoskeletal system: Obtain an arteriogram if vascular injury is suspected (e.g., pulsating or expanding hematoma, distal perfusion deficit). Obtain radiographs as needed for extremity injuries. Knee dislocations (not patellar dislocations) require a CT angiogram to rule out popliteal artery injury.
• Management of emergent procedures Cricothyroidotomy: Can't ventilate? Can't intubate?  Flail chest: Serial rib fractures in at least 2 places create a paradoxically moving chest wall. The patient will likely require intubation to assist with breathing. Needle thoracostomy: Inserting a chest tube takes several minutes. A 14-gauge needle to the second intercostal space midclavicular line takes seconds. Cardiac tamponade: If seen on ultrasound with tamponade physiology, perform pericardiocentesis. If possible, insert a "pigtail" into the pericardium, as the bleeding will likely reaccumulate. Tube thoracostomy (aka "chest tube"): The treatment for pneumothorax and hemothorax. Emergent thoracotomy: For patients in extremis with suspected penetrating injury to the heart or disruption of major vessels (aorta, pulmonary artery).
• Ankle injuries Traumatic ankle injuries are among the most common orthopedic complaints encountered in the ED. The spectrum of injury ranges from sprains (microscopc damage to a ligament) to significant fracture requiring operative intervention. In general, the Ottawa ankle rules guide the clinician in determining which patients need radiographic imaging. X-rays of the ankle and/or foot are indicated in the presence of:- Tenderness over the distal 6 cm of the posterior tibia or fibula- Tenderness over either malleolus- Inability to bear weight over 4 steps- Tenderness over the base of the fifth metatarsal- Tenderness over the navicular bone If there is concern for syndesmotic disruption between the tibia and fibula, rupture of the deltoid ligament, or ankle instability due to fractures, stress views of the ankle should also be added (x-ray in supination/external rotation).
• Knee injuries Knee pain is another common reason patients present to the ED. Several exam maneuvers should be performed to assess for certain injuries.- A locking sensation on passive range of motion may be a sign of meniscal injury.- Active range of motion not resulting in full extension can indicate quadriceps tendon rupture.- The anterior/posterior drawer test assesses ACl and PCL integrity.- Varus/valgus stress assesses the integrity of the medial/lateral collateral ligaments. Knee dislocation in obese patients may occur after only minor trauma and may self-reduce before presentation to the ED.
• Hip injuries The differential for hip pain is highly dependent on the age of the patient.- Children and adolescents (particularly if they are obese) are at risk for a slipped capital femoral epiphysis or Legg-Calvé-Perthes disease (avascular necrosis of the femoral head; typically affects children 4-8 years of age). If the hip pain was preceded by a recent URI, the patient may be suffering from toxic synovitis. Keep in mind that the presenting complaint for hip issues in children may be knee pain.- Older patients are at high risk for "hip fractures" (technically a proximal femur fracture) 2° to osteopenia. Classically, the affected limb is shortened and externally rotated. Other causes of hip pain include osteoarthritis and trochanteric bursitis. In addition, patients of all ages are at risk for hip dislocation.- A tremendous amount of force is required to dislocate the hip join, and dislocation typically occurs only when the hip is flexed at the moment of impact (e.g., knee vs dashboard in a MVA).- Typically the ligamentum teres artery is severed in the process, placing the patient at risk of developing avascular necrosis of the femoral head as a delayed complication. All joints in the body are at risk for septic arthritis, which involves direct inoculation of the joint or hematogenous spread of pathogens. - Patients may be febrile with exquisit tenderness on ranging the join.- Labs show an ↑ WBC count, CRP, and ESR.- Joint aspirate with a WBC > 100,000/mm3 is compatible with septic arthritis.- Treatment consists of IV antibiotics and joint washout by an orthopedic surgeon.
• Orthopedic pearls Tenderness over the scaphoid bone requires splinting even if inital x-rays are negative. A scaphoid fracture may take several days to become visible on x-rays. Compartment syndrome typically features good pulses and sensation until it reaches an advanced state. Excruciating pain with passive movement is the earliest sign. An ankle injury may lead to a knee injury (Maisonneuve fracture). Shoulder dislocations may lead to axillary nerve injury. Supracondylar fractures in children may lead to radial nerve injury. Clavicle fractures are typically treated conservatively with a sling. The first rib, proximal clavicle, sternum, scapula, and femur require signifiant force to fracture. Look for other injuries.
• Unstable bradycardia Symptomatic bradycardia is usually due to 1 of the following:- High vagal tone (cholinergic activity, inferior MI, digoxin toxicity)- Conduction abnormalities (sick sinus syndrome, AV-nodal blocks, diseases such as Lyme carditis or multiple myeloma)- Medication effects (β-blockers, calcium channel blockers) The underlying cause influences the efficacy of the treatment approach:- High vagal tone responds to atropine.- Conduction abnormalities often require a manual override of the conduction system (e.g., pacing) - Unfortunately, conditions such as β-blocker overdose lead to ↓ chronotropy and ↓ inoptropy. In many cases, even pacing remains ineffective. Treatment:- A patient found to be in unstable bradycardia (HR < 60) with sympomatic hypotension (e.g., chest pain, changes in mental status, or other signs/symptoms of shock) requires treatment. While preparing for pacing, administer atropine 0.5 mg IV q 3-5 min x 3.- There are 3 ways to pace a patient:→ Transcutaneously: Place pads on the chest/back, set to the desired rate, and ↑ amperage until you have mechanical capture. If possible, sedate.→ Transvenously: Place a cordis central line and float a pacing wire to the heart. This takes about 15 minutes but provides the most definitive management until a permanent pacemaker can be placed.→ Chemically: Dopamine 2-10 µg/kg/min or epinephrine 2-10 µg/min.
• Cardiac arrest In the event of cardiac arrest, start CPR immediately using end-tidal CO2 to monitor quality. As CPR is being performed, begin bag-valve-mask ventilation, rapidly obtain vascular access (or interosseous access), and attach defibrillator pads to the patient. At the first rhythm check, you will find 1 of 4 electrical patterns: VF, pulseless VT, asystole, or PEA.- Asystole or PEA: CPR and epinephrine. No defibrillation, atropine, or pacing.- VF/pulseless VT:→ CPR with epinephrine q 3-5 minutes + defibrillation with 200 J (biphasic) or 360 J (monophasic) + an antiarrhythmic agent (amiodarone 300 mg IV once followed by a 150 mg dose in 3-5 minutes if still in a shockable rhythm).→ If torsades to pointes develops, give magnesium 1-2 g IV.- Identify and treat the H's and T's:→ Hypothermia → warm them up.→ H+ (acidosis) → reverse acidosis.→ Hypo-/Hyperkalemia → either give or remove K+.→ Hypoxia → 100% O2; secure/establish airway.→ Hypovolemia → fluid replacement.→ Thrombosis (PE, MI) → thrombolytics.→ Tamponade → pericardiocentesis.→ Tension pneumothorax → needle decompression.→ Toxins → antidote (e.g., hydroxocobalamin in cyanide toxicity).
• Tachycardia Tachycardia is defined as a heart rate > 100 bpm. Sinus tachycardia has an underlying cause that must be addressed (e.g., dehydration, fever, pain). The treatment of sinus tachycardia with rate-limiting agents is likely harmful, as the heart rate was compensatory to an underlying process and the compensatory mechanism is removed. Tachyhysarrythmias can result from:- Self-sustained conduction pathways (e.g., SVT)- Multiple foci of automaticity (atrial flutter, AF)- Ventricular focus (VT) Treatment:- A patient with unstable tachycardia (e.g., shortness of breath, chest pain, hypotension, ischemic ECG changes) requires immediate synchronized cardioversion. Stable patients can be treated medically.- In stable tachycardia, attempt vagal maneuvers first and then escalate therapy as follows:→ Narrow, regular complex (e.g., SVT): Adenosine→ Narrow, irregular complex (e.g., AF): Rate control (metoprolol, diltiazem)→ Wide complex (e.g., VT): Amiodarone→ All of the above rhythms can be electrically cardioverted if medical therapy fails.- Special cases:→ Do not cardiovert stable AF that has been present for > 48 hours. Get a TEE first to assess for atrial thrombus.→ In torsades de pointes, give magnesium 1-2 g IV and provide either chemical or electrical overdrive pacing (may resolve with ↑ heart rate).
• Toxicology In general, there are several things you need to inquire about to obtain when treating a poisoned patient:- Time and type of ingestion- Quantity and route of ingestion- Comorbidities- Vitals- ECG- Pupils, bowel sounds, skin exam, reflexes, and clonus- Respiratory/heart rate, mental status
• Advertisement
• Toxicology pearls - Do not intubate patients with aspirin toxicity unless you absolutely must. Because the mechanical ventilator will match these patients' high minute volumes, they will become more acidotic and die. - In all overdoses, send an acetaminophen level. - In smoke inhalation, consider carbon monoxide and cyanide toxicity. - Serotonin syndrome kills. - Neuroleptic malignant syndrome can look like serotonin syndrome but develops more slowly (> 24 hours) and features regidity rather than clonus. - If a patient appears altered or intoxicated, don't forget to check a blood sugar. - Lithium toxicity may require dialysis. - Digoxin toxicity may require antibody fragment administration (Digibind). - Charcoal is useful only in ingestions that occurred < 60 minutes ago. Multidose activated charcoal can be given for "gut dialysis" (removal of toxins from the enterohepatic circulation). - Whole bowel irrigation (similar to colonoscopy prep) is indicated for "body packers" and for children with visible lead paint chips on x-ray, as well as for certain other ingestions.
• Abdominal aortic aneurysm (AAA) Risk factors: Age > 60, atherosclerosis, and smoking. Underlying mechanisms are as follows:- Weakness in the connective tissue of the tunica muscularis leads to bulging out of the vessel, typically inferior to the origin for the renal arteries.- Wall stress is directly correlated to diameter (Laplace's law); once a critical threshold is passed, the aneurysm will rupture. Rupture occurs into the retroperitoneal space, which can hold enough blood volume to cause the patient to exsanguinate within minutes. Symptoms/Exam:- Presents with back pain/abdominal pain and syncope.- Leg pain/paresthesias 2° to occlusion of the artery of Adamkiewicz leads to spinal cord infarcts. Diagnosis:- Physical exam may show an abdominal bruit or a palpable pulsatile abdominal mass.- Ultrasound can assess for the presence of AAA but not rupture.- CT angiography of the abdomen/pelvis can detect rupture. Treatment:- A ruptured AAA requires immediate resuscitation and emergent operative repair.- Several large-bore (14- to 16-gauge) IVs should be inserted with type O blood running via a level-1 transfer (can administer 1 unit of blood over 30 seconds).- Reverse coagulopathy.- Do no manipulate BP with pressors (more pressure = more bleeding).
• Sexual assault Begin by diagnosing and treating the victim's physical and emotional injuries. Then collect legal evidence and document that evidence carefully. Your main concern should always be the well-being of the patient. Information should include the following:- Ascertain any injuries sustained during the assault.- Determine the risk of pregnancy. When was the last menstrual period? Any birth control?- Find out where, when, and how the assault occurred. What happened during the assault? Determine the number of assailants; the use of force, weapons, objects, or restraints; which orfices were penetrated; and whether alcohol and/or drugs were involved.- Determine what happened after the assault. Are there any specific symptoms or pains? Did the patient bathe, defecate, urinate, brush teeth, or change clothes? Has the patient had sexual intercourse in the last 72 hours? Diagnosis:- Assess for pelvic trauma that may require immediate intervention.- The collection of physical evidence (e.g., debris, fingernail scrapings, dried secretions from the skin, pubic hairs) is often restricted to certified personnel.- Medically indicated tests include a pregnancy test; nucleic acid amplifcation testing the gonorrhea and chlamydia; a wet mount and culture for trichomoniasis, bacterial vaginosis, and candidiasis; serology for syphilis; and HBV/HIV testing. These tests will be - in patients who present early after the assault and may need to be repeated later. Treatment:- Treat traumatic injuries.- Infection prevention:→ Gonorrhea and chlamydia prophylaxis.→ HIV prophylaxis and high-risk populations.- Pregnancy prevention:→ Administer 2 ethinyl estradial/norgestrel (Ovral) tablets PO immediately and again 12 hours later.→ Offer counseling.
• Animal and insect bites The management of bite wounds requires a fine balance between reducing the risk of infection and achieving cosmesis. Patients are often surprised when they do not receive sutures for wounds that they feel should be closed.- Animal bites result in tissue destruction and inoculation of the wound with oral flora. Depending on the animal, the patient may be at risk for a variety of complications.- Dog bites produce large, torn wounds (bite and then shake/pull).- Dogs have relatively clean mouths, so wounds may be sutured unless they are on the hand.- Cat bites cause deep penetrative wounds (high anaerobic infection risk).- The kicking action of a cat's hind legs may lead to inoculation with Bartonella henselae. Treatment:- Antibiotic prophylaxis should be provided even if the wound is not repaired. Amoxicillin/clavulanate or a similar agent that covers oral flora is preferred.- Wounds should be irrigated at high pressure with copious amounts of fluid. A wound may be loosely approximated rather than sutured tightly to prevent further wound contamination without creating an aerobic environment.- New CDC recommendations on the treatment of rabies are as follows:→ If the animal can be observed and does not display symptoms of rabies after 10 days, no vaccine is necessary.→ If the patient slept in the same room as a bat, vaccinate.→ There have been no documented cases of rabies transmitted by a rodent (including squirrels).→ Don't forget to address wound care and tetanus status.→ Give immunoglobulin to all patients who were not previously immunized. If possible, inject half around the bite and half IM elsewhere.→ Vaccine should be administered in 4 doses on days 0, 3, 7, and 14.→ Those previously vaccinated need only 2 vaccine doses.→ Immunocompromised patients still get 5 doses of the vaccine.
• Tetanus Trismus (i.e., lockjaw), glottic spasm, and convulsive spasms caused by Clostridium tetani. High-risk patients include the elderly (due o inadequate immunizatio), IV drug users, and skin ulcer patients.- The tetanus toxin affects modulatory motor neurons that normally secrete GABA to suppress motor impulses. As GABA levels in the synpatic cleft decline, even small accidental impulses will produce muscle contractions. This results in a generalized tonic state in which all striated muscles begin to contract.- Because the posterior muscle groups of the torso are stronger than the anterior groups, patients in the most advanced disease states are often arched with contract arms (the biceps is stronger than the triceps). This is called opisthotonos.- Although the heart muscle is not affected, tetanus may lead to respiratory arrest, hyperthermia and rhabdomyolysis, and subsequent death. Treatment:- Benzodiazepines to control muscle spasms; neuromuscular blockade if needed to control the airway.- Metronidazole is the antibiotic of choice.- Single IM dose of human tetanus immunoglobulin (HTIG)- Tetanus toxoid-containing vaccine: for example, TdaP, Td, DTaP, DT, depending on age, previous immunization, or allergies → Inject in separate site from HTIG Vaccination:- For children < 7 years of age→ DTaP (diphtheria, tetanus, and acellular pertussis)→ DT (diphtheria, tetanus): for children who cannot tolerate the pertussis vaccine- For adolescents and adults:→ Tdap (tetanus, diphtheria, pertussis): recommended for patients 11-64 years of age, but may be considered for children > 7 years old→ Td (tetanus, diphtheria): for patients > 11 years old
• Anaphylaxis Patients who are presensitized to certain antigens may develop a significant type I hypersensitivity (allergic) reaction on exposure). True anaphylaxis is associated with significant mortality, usually form airway occlusion rather than from anaphylactic shock (which is easily treated with IV fluids and pressors).- IgE-mediated cytokine release in response to an antigen triggers a variety of reactions. The predominant cytokine is histamine. Histamine can also be released independent of IgE by direct mast cell stimulation (e.g., morphine, IV contrast dye).- In addition to vasodilaion, the capillary bed becomes leaky and significant edema ensues. Edema may occur superficially (facial swelling), in the gut (leading to nausea/vomiting/abdominal pain), and in the airway (placing the patient at risk for airway occlusion). The latter is exacerbated by induced bronchospasm as well as bronchorrhea.- Anaphylaxis also leads to systemic vasodilation, resulting in hypotension despite high cardiac output (distributive shock). Diagnosis:- A clinical diagnosis. Patients often present with significant hives and obvious swelling along with a history of allergic reactions.- To meet the diagnostic criteria for anaphylais, 2 organ systems must be involved (e.g., hives and abdominal pain or vomiting). No lab tests or imaging studies aid in diagnosis. Treatment:- IM epinephrine.- Histamine blockade (IV diphenhydramine for H1 blockade; famotidine for H2 blockade).- Methylprednisolone- Nebulized albuterol (for wheezing).- Early intubation if necessary.
• Angioedema There are 2 types of angioedema: hereditary and acquired (e.g., related to ACEIs). The condition becomes an emergency if it involves the tongue or upper airway. Underlying mechanisms include:- The complement system is a cascade that ends in the formation of a "membrane attack complex" (MAC), which disrupts the cell walls of pathogens. C1 is the first step in this cascade. In hereditary angioedema, C1 is not inhibited, so it may inappropriately trigger the cascade.- An autosomal dominant mutation leads to a deficiency of C1 esterase (aka C1 inhibitor). C1 then becomes overactive, leading to the production of kallikrein. Subsequently, kininogen and therefore bradykinin levels can be ↑.- Bradykinin enhances vascular permeability, which in turn produces significant tissue edema. ACEIs also ↑ bradykinin. Diagnosis:- Diagnosis is clinical.- C1 esterase inhibitor levels confirm the diagnosis but are not available for immediate decision making in the ED. Treatment:- Most treatment modalities available for anaphylaxis have no effect on the course of angioedema.- Provide airway proteciton.- Fresh frozen plasma (FFP) contains C1 esterase inhibitor and may ↓ the severity of hereditary angioedema.- Concentrated C1 esterase inhibitor is available but is costly.
• Frostbite Severe localized tissue injury due to freezing of interstitial and cellular spaces after prolonged exposure to very cold temperatures. Pathogenesis: Damage occurs via direct cold-induced cell death as well as delayed inflammation from reperfusion injury. Electrolyte flux can also occur if intracellular ice crystals form. Superficial: Injury to cutaneous and subcutaneous tissue. Skin is soft under a frozen surface. Large, clear, fluid-filled vesicles develop within 2 days (indicating a good prognosis); sloughing leaves new skin that is pink and hypersensitive. Deep: Injury to the above tissues plus deep structures (muscle, bone). Skin is hard under a frozen surface. Treatment: - Remove wet clothing; avoid walking on frostbitten feet- Evaluate for concurrent hypothermia and treat that first!It is imperative that rewarming begins at the trunk. Immediate warming of the periphery results in peripheral vasodilation, causing cold acidemic blood to return to the trunk, which can lead to life-threatening arrhythmias!- Rewarming→ Passive: remove wet clothing, cover with blankets, warm room (preferably 28°C)→ Active: immerse affected extremity in a warm (preferably 37-39°C) circulating water bath- Analgesia and tetanus prophylaxis- Manage suspected infections aggressively with antibiotics and sterile dressings
• Hypothermia Defined as a core body temperature of < 35°C (95°F). Etiology: Environmental exposure, alcohol ingestion, drugs (barbiturates, benzodiazepines, narcotics), hypoglycemia, CNS or hypothalamic dysfunction (via loss of stimulus of shivering response and adrenal activity), hypothyroidism, skin disorders, and sepsis. Diagnosis:- ECG (best initial test): prolongation of all ECG intervals; elevated J point (characteristic J or Osborn wave)- Imaging: chest x-ray to exclude pulmonary edema or aspiration pneumonia; CT if head trauma suspected- Laboratory tests: complete metabolic panel, complete blood count, or arterial blood gas to exclude bleeding diathesis and early organ dysfunction Treatment:- Resuscitation (ABCDE approach); place two large (14 or 16 gauge) peripheral IVs. - Rewarming→ Passive external: Blankets should be used only in patients who shiver. Once shivering stops, the patient no longer generates heat, and additional methods of rewarming must be used.→ Active external: Warmed blankets, warm-air circulatory blankets, hot-water bottles.→ Active internal: Warm humidified O2; heated IV fluids; gastric, colonic, bladder, or peritoneal lavage; thoracic lavage; extracorporeal rewarming.- Do not pronounce patients dead until they have been rewarmed to 35° C; full recovery is not uncommon.
• Heat emergencies Heat exhaustion:- Extreme fatigue with profuse sweating. Also presents with nausea/vomiting and a dull headache.- Exam: Body temperature is normal or slightly ↑. Patients are tachypneic, tachycardic, and hypotensive.- Treatment: Treat with IV saline and a cool environment. Heat stroke:- Elevation of body temperature above normal as a result of temperature dysregulation (> 40° C). A true emergency. Monitor for convulsions and cardiovascular collapse.- Exam: Patients with ↑ body temperature, altered mental status, and possible paradoxical shivering. Patients have hot, dry skin, often with no sweating. Ataxia may be seen.- Treatment: Treat with aggressive cooling. Remove from the heat source and undress. Use an atomized tepid water spray in combination with fans (can cool as fast as 0.5°C/min), and apply ice packs to the groin, axillae (some facilities use cooled IV fluids run through a central line).- Treat neuroleptic malignant syndrome and drug fever with dantrolene. Treat seizures with diazepam.
• Burns Burns are injuries to tissue caused by heat, chemicals, and/or radiation. Etiology:- Thermal injury (e.g., scalding, contact with a hot surface, fires)- Non-thermal injury: radiation, chemical burns, electrical burns Local effects:- Almost all burns are colonized by bacteria.  - Common pathogens that infect burn wounds: MRSA, Pseudomonas, Klebsiella, Acinetobacter, Candida- Eschars can cause constrictive effects.→ Significant eschar on chest or neck → restricts chest excursion → asphyxia→ Circumferential eschars → loss of skin elasticity → impaired blood flow and/or compartment syndrome (caused by an accumulation of fluids) → acute ischemia distal to the eschar   Systemic effects:- Large (> 30% of the body surface area) and/or deep burns → systemic inflammatory response syndrome→ Generalized edema, acute respiratory distress syndrome, and hypovolemic shock with paralytic ileus→ Disseminated intravascular coagulation (DIC)- Evaporative fluid loss → hypothermia, dehydration- Hemolysis, muscle damage → hemoglobinuria and/or myoglobinuria → acute tubular necrosis- Immunosuppression- Hypermetabolic state with increased nutritional requirements- Inhalation of hot smoke and/or noxious gases → inhalation injury → Laryngeal edema → airway obstruction→ Pneumonitis→ Carbon monoxide poisoning→ Cyanide poisoning 1st degree (superficial burn): Pain, erythema, swelling- The burn wound blanches on applying pressure and refills rapidly- Healing within 3-6 days without scarring 2a degree (superficial partial-thickness burn): Pain, erythema, vesicles/bullae- The burn wound blanches on applying pressure and refills slowly.- Healing within 1-3 weeks with hypopigmentation/hyperpigmentation but without scarring 2b degree (deep partial-thicknessburn): Minimal pain, mottled skin with red and/or white patches, vesicles/bullae- The burn wound does not blanch on applying pressure.- Healing takes 3 weeks or longer and results in scar formation 3rd degree (full thickness burn): No pain, tissue necrosis with black, white, or gray leather-like skin (eschar), no vesicles/bullae- Epidermis, dermis, and subcutaneous tissue.- The burn wound does not blanch on applying pressure.- The burn does not heal by itself. 4th degree burn: Deeper structures (muscles, fat, fascia, and bones)- Charred tissue- The tissue is dead and requires amputation. In the case of adults, shock sets in when burns involve > 15% of the body surface. Diagnostics:- Pulse oximetry: monitor for hypoxemia  - Blood gas analysis: monitor for hypoxemia, metabolic, and/or respiratory acidosis- Serum electrolytes: hyperkalemia and hyponatremia occurs in the acute phase following burns; hypernatremia may occur later. - If inhalational injury is suspected → Bedside respiratory function tests to rule out airway obstruction, chest x-ray in order to rule out ARDS, carboxyhemoglobin levels, end tidal CO2 (ETCO2), serum lactate, flexible fiberoptic laryngoscopy/bronchoscopy  - BUN/creatinine: monitor for acute renal injury- Hemoglobin, hematocrit: monitor for hemolysis- Serum protein and albumin levels  - If wound infection or sepsis is suspected: wound swab and blood cultures- In circumferential limb wounds at risk for distal ischemia/compartment syndrome, assess perfusion with pulse oximetry (> 90% indicates adequate perfusion) and assessment of capillary refill and peripheral pulses Treatment:- Airway management: intubation and high flow oxygen therapy is indicated if an inhalation injury is suspected or if burns involve more than 30-40% of the body surface- Begin initial fluid resuscitation with crystalloids, usually lactated Ringer's solution (RL) → Current recommendations: volume of lactated Ringer's solution to be administered within a period of 24 h = 2 mL x % of body surface involved in 2nd and 3rd-degree burns x body weight (in kg)→ Half of this volume should be administered within the first 8 hours and the remaining half within the next 16 hours→ Children < age 14: Volume of lactated Ringer's solution to be administered within a period of 24 h = 3 mL x % of body surface involved in 2nd and 3rd-degree burns x body weight (in kg)- Remove any burnt clothing- Cool the burnt area with cool running water or saline-soaked gauzes. Do NOT use ice or ice water! Cover the wound with a sterile dressing. Core body temperature should be monitored for hypothermia.- Tetanus prophylaxis- Analgesia (opiates often necessary) - Proton pump inhibitors or H2 antagonists: prophylaxis against Curling's ulcers- Prophylactic systemic antibiotic therapy is NOT routinely recommended.
• Management 1st and 2nd degree burns - Irrigation - Topical moisturizers (e.g., calamine lotion) or aloe vera-based gels: relieve symptoms of 1st-degree burns - Consider antiseptic ointments (e.g., silver sulfadiazine, mafenide) or topical antibiotics (bacitractin; triple antiobitic ointments are a combination of bactracin neomycin, polymyxin B) - For periorbital or periocular burns, topical antibiotics (e.g., bacitracin, neomycin, or erythromycin) are preferred over silver sulfadiazine, which may be irritating and cause ocular toxicity. - Deroofing bullae/vesicles   - Dressing is indicated in partial thickness (2nd-degree) burns.
• Management of 3rd and 4th degree burns - Early debridement of burnt, necrotic tissue   - Method of tissue coverage varies depending on the specific burn characteristics. Options include:→ Free skin grafts (split-thickness or full-thickness)  → Flap reconstruction with free or pedicled flaps.   - Topical antibiotics (e.g., silver sulfadiazine, bacitracin, neomycin)
• Electrical injury - Fatal in up to 30% of cases; cardiac arrest due to arrhythmias is the most common cause of death - 70% of survivors have permanent damage (e.g., chronic pain syndromes). - Lightning strikes can be demonstrated as a cause of death based on the following:→ Lichtenberg figure: branching (fern‑like) patterns on the skin  → Large burns or groups of small burns that appear similar to gunshot wounds→ Scorched hair on the scalp→ Findings on clothing: Grouped holes in the individual's clothes, laceration of leather and shoe soles, traces of melting on the body from metal (belt buckles, wrist watches) - Metalization of the skin: At the point of electrical contact, there is evidence of volatilization and deposition on the skin from metal that was located at the time on the body (evidence via histochemistry or atomic absorption spectrometry). Treatment:- CABs as above; IV fluids for severe burns.- Administer pain medications and treat burns.- In mass casualty events (e.g., a lightning strike into a crowd), perform reverse triage and prioritize pulseless patients, as return of spontaneous circulation (ROSC) is very likely.- Treat myoglobinuria with IV fluids to maintain a urine output of 1.5-2.0 cc/kg/hr.- Tetanus prophylaxis.- Asymptomatic patients with low-voltage (< 1000-V) burns can be discharged.
• Corneal abrasion Definition: scrape or scratch injury on the corneal epithelium Epidemiology: most common eye injury Etiology:- Injury from an object (e.g., tree branch, fingernail, ball, mascara brushes) hitting, flying into, or poking the eye- Foreign matter stuck under the eyelid  - Entropion- Prolonged contact lens wear or improperly fitted lenses- UV light (i.e., UV keratitis)- Thermal burns (e.g., cigarettes, matches)- Trachoma- Dry eyes (e.g., Sjogren syndrome) Clinical findings:- Foreign body sensation in the eye- Eye pain- Epiphora- Blurred vision- Photophobia- Conjunctival injection Diagnostics: examination of the eye using fluorescein staining   Treatment:- Removal of any retained foreign object- Analgesia: oral NSAIDs, topical NSAIDs (e.g., diclofenac, ketorolac), or narcotics, depending on pain severity - Infection prophylaxis  → In the general population: antibiotic eye drops or ointment (e.g., erythromycin)→ In contact lens wearers: antibiotic eye drops or ointment with antipseudomonal activity (e.g., ciprofloxacin) Prognosis: Small, uncomplicated corneal abrasions: rapid healing of the epithelium expected within approx. 24-48 hours; no followup necessary
• Chemical conjunctivitis Caused by acid or alkali exposure. Diagnosis: Determine pH from litmus paper. - Coagulation necrosis is associated with acid burns, liquefaction necrosis with alkali burns. Treatment: Treat with copious irrigation with a Morgan lens until pH approaches neutral (keep in mind that the pH of normal saline is about 5.5, so you will never get the pH to be 7 no matter how much you irrigate).
• Radiology modalities CT with contrast: Abdominal abscess, abdominal trauma, aortic aneurysm/dissection, appendicitis, bowel perforation, chest mass/trauma, colitis, diverticulitis, hemoptysis, hydronephrosis, intestinal obstruction, persistent hematuria, PE, tumor diagnosis/staging. CT without contrast: Head trauma (including skull racture), intracranial bleed, nephrolithiasis, suspected spinal trauma/fracture. MRI with contrast: Brain/spinal tumor/infection, joint imaging, MS, osteomyelitis, vascular imaging, spinal cord compression. Plain film: Chest mass/trauma, hemoptysis, intestinal obstruction/perforation, most orthopedic problems, pneumonia. Duplex ultrasound: Carotid stenosis, DVT. Ultrasound: AAA screening, appendicitis (in pediatric/pregnant patients), gallstones/cholecystitis, hydronephrosis, intussusception, liver screening, pregnancy/most gynecologic pathology, pyloric stenosis, scrotal pathology (torsion, hydrocele, epididymitis/orchitis, scrotal mass). Barium swallow: Esophageal obstruction. Barium enema: Colonic masses (single contrast), IBD/diverticulosis (double contrast). Upper (or lower) endoscopy: Esophageal obstruction, hematemesis, PUD, upper (or lower) GI bleeding. Cystoscopy: Persistent hematuria. HIDA scan: Cholecystitis.
• Compartment syndrome Compartment syndrome is a condition in which increased pressure within a muscle compartment (containing nerves and vasculature, enclosed by unyielding fascia) leads to impaired tissue perfusion. Early presentation: - Pain→ Often out of proportion to the extent of injury→ Worse with passive stretching or extension of muscles→ Very tight, “wood-like” muscles that are extremely tender to touch- Paresthesia (e.g., pins and needles)- Soft tissue swelling- Initially, peripheral circulation and distal pulses are maintained. Late presentation: - Muscle weakness to paralysis  - Absent (or weak) distal pulses  - Cold peripheries- Pallor or cyanosis Diagnostics:- Compartment pressures (initial and confirmatory test): measurement of tissue pressure with a manometer and calculation of delta pressures (delta pressure = diastolic - (compartment) tissue pressure)→ Delta pressure in manifest compartment syndrome: ≤ 30 mm Hg  - Laboratory tests specific for rhabdomyolysis- X-rays   Surgical treatment: required for all cases of acute compartment syndrome!
• Blunt chest trauma Possible injuries:- Chest wall injuries: rib fracture, flail chest, sternal fracture- Aortic injury (highest lethality rate!)- Cardiac contusion and pericardial effusion and cardiac tamponade- Pulmonary contusion- Hemothorax- Pneumothorax- Tracheobronchial injury- Diaphragmatic rupture- Esophageal rupture Clinical features:- Chest pain- Hypotension, tachycardia, hypoxia- Diminished breath sounds in pneumothorax- Jugular venous distention could suggest pericardial effusion or cardiac contusion Approach to blunt chest trauma:1. Primary survey: prehospital trauma care and preliminary trauma care in the hospital2. Emergency assessment: of hemodynamically unstable patients to rule out life-threatening conditions  3. Rapid diagnostic evaluation- Chest x-ray - Ultrasound (extended FAST)  - Echocardiography and ECG- Others: CT, transesophageal echocardiography (TEE), bronchoscopy, angiography Management:- Close monitoring of vital signs- Appropriate surgical repair after stabilization of vitals  - Unstable patient: immediate surgery/explorative thoracotomy

back  |  next 1 / 1