Author: Joseph Ciano, USA

Joey Ciano, DO, MPH is an Emergency Medicine Physician from New York, USA. He completed his Emergency Medicine Residency in Brooklyn, NY and a Fellowship in Global Emergency Medicine in the Northwell-LIJ Health System. He is interested in building the educational infrastructure of EM in countries where EM is not yet recognized as a field and in countries that are in the early stages of this process. He has partnered with international NGOs in EM educational projects and works as a visiting EM faculty member in West Bengal, India. He is excited to collaborate with the other authors of the iEM Education Project to contribute to world of FOAM-ed.

Question Of The Day #88

question of the day
~ Joseph Ciano, USA ~ Leave a comment
Which of the following is the most appropriate next step in management?
  • A) Methotrexate for ruptured ectopic
  • B) IV Antibiotics
  • C) Transvaginal ultrasound
  • D) Consult OBGYN for operative management

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with shortness of breath and abdominal discomfort for 1 day.  On exam, she is hypotensive, tachycardic, and tachypneic.  Her lungs are clear, the abdomen is tender and distended, and the pregnancy test is positive.  This patient has a ruptured ectopic pregnancy until proven otherwise and requires prompt surgical management.  Once diagnosed by the Emergency clinician, ectopic pregnancy can be managed medically or surgically.  See the chart below for more details.

Treatment options for ectopic pregnancy

 

Medical Management (Methotrexate) Indicated:

Surgical Management

Indicated:

Patient hemodynamically stable

Patient hemodynamically unstable

HCG <5,000

HCG >5,000

Able to comply with Methotrexate treatment and follow up

Unable to comply with Methotrexate treatment and/or follow up

No fetal cardiac activity on ultrasound

Fetal cardiac activity present on ultrasound

   

This patient has an assumed ectopic pregnancy due to the positive pregnancy test and presence of hemodynamic instability.  A transvaginal ultrasound (Choice C) would help definitively diagnose the patient with a ruptured ectopic pregnancy, but this should not delay consultation with the OBGYN team for definitive surgical management.  Methotrexate (Choice A) is a medical treatment for ectopic pregnancy, but Methotrexate is contraindicated in ruptured ectopic due to the need for surgical treatment and intra-abdominal hemorrhage control.  IV antibiotics (Choice B) are often given preoperatively for infection prophylaxis (prevention), but this is not a crucial next step.  This patient is in shock and needs operative management. The best next step is OBGYN consultation for operative management (Choice D).

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Question Of The Day #87

question of the day
~ Joseph Ciano, USA ~ Leave a comment

 

Test Value

Reference Range

BUN

14

6 – 24 mg/dL

Creatinine

0.87

0.59 – 1.04 mg/dL

Hemoglobin

5.5

12.0 – 15.0 g/dL

WBC count

5.2

4.5 to 11.0 × 109/L

HCG quantitative

0

<5 mIU/mL

Which of the following is the most like cause for this patient’s condition?
  • A) Asthma
  • B) Ruptured ectopic pregnancy
  • C) Heavy menses
  • D) Pulmonary embolism

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with shortness of breath with deceased exercise tolerance or 5 days.  Her vital signs are normal and lungs are clear, but she appears pale.  The laboratory test provided shows normal kidney function, a negative serum pregnancy test, and a markedly low hemoglobin level.  A ruptured ectopic pregnancy (Choice B) can cause shortness of breath due to anemia and hemorrhagic shock, but this patient has a negative pregnancy test.  Asthma (Choice A) is unlikely given the patient’s normal lung exam without wheezing and no mention of cough.  A pulmonary embolism (Choice D) is possible due to the tachycardia, but the patient lacks other risk factors as stated in the question stem.  A D-Dimer test could help further evaluate if this patient has a pulmonary embolism, but the low hemoglobin likely explains the patient’s symptoms.  The patient’s history of menorrhagia, also known as heavy menses (Choice C), is a common cause of anemia in women of childbearing age.  Even though this patient is not currently menstruating, her heavy menses are the most likely cause for her shortness of breath.  Choice C is the best answer.

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Question Of The Day #86

question of the day
~ Joseph Ciano, USA ~ Leave a comment
420 - right pneumothorax1
Which of the following is the most appropriate next step in management for this patient’s condition?
  • A) IV Heparin bolus and infusion
  • B) Supplemental oxygen
  • C) Needle decompression to right chest
  • D) IV Azithromycin

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with acute onset shortness of breath with pleuritic right sided chest pain.  On exam, there is mild tachypnea and a borderline low SpO2 of 95% on room air.  The chest X-ray demonstrates a small right sided pneumothorax (see location of red stars below).

Needle decompression to the right chest (Choice C) would be the right choice if the patient had a right sided tension pneumothorax.  Signs of a tension pneumothorax are hypotension, tachycardia, tracheal deviation, and mediastinal shift on Chest X-ray.  Tension pneumothorax should be diagnosed clinically without a chest X-ray and promptly treated with needle decompression with a 14-16 gauge needle at the 2nd intercostal space in the mid clavicular line.  Needle decompression can also be performed at the 4th or 5th intercostal space in the anterior axillary line. Needle decompression is always followed by placement of a formal chest tube.  This patient does not have the hemodynamic instability or chest X-ray findings of a classic tension pneumothorax. IV Azithromycin (Choice D) would be appropriate for a COPD exacerbation or for community-acquired pneumonia.  This patient does have a cough, but lacks fever, sputum production, and also has a pneumothorax on X-ray that can explain his symptoms.  An IV Heparin bolus and infusion (Choice A) would be the ideal treatment for a pulmonary embolism or acute coronary syndrome.  Again, the Chest X-ray provided shows support for an alternative cause for the patient’s symptoms.  The best next step is supplemental oxygen (Choice B).  100% supplemental oxygen helps decrease the time to lung expansion in patients with pneumothoraces.   A nonrebreather mask at 15L/min is the ideal method to providing this level of oxygen.

This patient has a small pneumothorax (<3cm between lung margin and chest wall).  Small primary pneumothoraces have two treatment options.  The first option is to administer 100% oxygen and place a pigtail catheter for rapid lung re-expansion.  The second option is to only administer 100% oxygen administration for a period of 4-6 hours followed by a repeat chest X-ray to evaluate for improvement of the pneumothorax.   If the pneumothorax is improving and symptoms are improving (less shortness of breath and chest pain), the patient can be discharged home with close outpatient follow up and no chest tube placement.  Deciding which treatment option is best should depend on the patient’s ability to follow up with a doctor, patient reliability, and resource availability.  This patient does have a small pneumothorax by measurement, but he likely has a secondary pneumothorax from his COPD.  Secondary pneumothoraces have a higher rate of recurrence and almost always require chest tube placement.  Regardless, the best initial step in treatment is supplemental oxygen (Choice B).

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Question Of The Day #85

question of the day
~ Joseph Ciano, USA ~ Leave a comment
SS Video 3 Pericardial Tamponade
Which of the following is the most likely cause for this patient’s condition?
  • A) Pulmonary embolism
  • B) Tension pneumothorax
  • C) Pneumonia with septic shock
  • D) Cardiac tamponade

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient presented to the Emergency department with 2 days of shortness of breath without chest pain, cough, or fevers.  The exam shows tachycardia, hypotension, mild tachypnea, clear lungs, and distant heart sounds.  Tension pneumothorax (Choice B) can cause hypotension and tachycardia and COPD is a risk factor for pulmonary bleb formation and rupture.  However, the lungs are equal and clear bilaterally, so this diagnosis is not likely.  Septic shock due to pneumonia (Choice C) is also less likely as there is no fever, the lungs are clear, and the patient lacks a cough.  The ultrasound image given also provides a clear explanation for the patient’s symptoms.  This patient is at risk for pulmonary embolism (Choice A) given his cancer history which can cause a hypercoagulable state and predispose him to clot formation.  Again, an understanding of the ultrasound image will provide the diagnosis.

The ultrasound image is a subxiphoid view of the heart demonstrating a pericardial effusion (red stars) with compression of the right ventricle (yellow arrow). 

This presentation is consistent with cardiac tamponade (Choice D).  Cardiac tamponade is a condition defined by the accumulation of fluid in the pericardial sac to the point of right ventricular collapse and obstructive shock.  Common presenting symptoms of cardiac tamponade include shortness of breath, chest pain, or nonspecific symptoms.  Risk factors for this diagnosis are penetrating chest trauma (hemopericardium), cancer (malignant effusion), lupus, end stage renal disease, uremia, HIV, Tuberculosis, or history of chest radiation.  The presence of hemodynamic instability (hypotension and tachycardia) is a hallmark of this condition, although early stages of tamponade can be seen on cardiac ultrasound before vital signs decompensate.  The patient may have Beck’s triad of muffled distant heart sounds, jugular venous distension, and hypotension, although the majority of patients with cardiac tamponade do not have all three of these signs together.  Treatment involves IV fluids, bedside pericardiocentesis (ultrasound guided preferred), and surgical pericardiotomy (“pericardial window”).

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Question Of The Day #84

question of the day
~ Joseph Ciano, USA ~ Leave a comment
475.3 xray abdomen series normal chest
Which of the following is the most appropriate next step in management for this patient’s condition?
  • A) IV insulin infusion
  • B) IV lactated ringers solution
  • C) Nebulized Beta-2 agonist
  • D) Endotracheal intubation

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient arrives to the Emergency Department with shortness of breath and generalized weakness or 3 days.  On physical exam, there is tachycardia, tachypnea, normal oxygen saturation, and a markedly elevated glucose.  The Chest X-ray provided is normal; there are no lung infiltrates or pleural effusions. 

This patient has diabetic ketoacidosis (DKA).  DKA is a serious condition of insulin deficiency characterized by hyperglycemia, metabolic acidosis, and ketosis.  Presenting symptoms include weakness, increased thirst (polydipsia), increased hunger (polyphagia), increased urination (polyuria), abdominal pain, or vomiting.  Shortness of breath can also be seen in DKA as the metabolic ketoacidosis triggers an increased respiratory rate to drive more exhaled carbon dioxide out of the body.  This deep rapid breathing seen in severe DKA is known as Kussmaul breathing.  The treatment of DKA involves IV fluids for hydration, insulin infusion, and close monitoring for electrolyte derangements (potassium abnormalities are common).  DKA patients are severely dehydrated due to osmotic diuresis from their hyperglycemic state.  For this reason, IV fluid resuscitation is the first step to DKA management.  Either normal saline or lactated ringers (Choice B) can be used, although large volumes of normal saline can worsen the acidotic state by causing a hyperchloremic metabolic acidosis.  Intravenous fluids should be started with a 20-30cc/kg bolus.  IV insulin infusion (Choice A) should never be started without a potassium level, and no potassium level is provided in the question stem.  Insulin lowers potassium, and administration of insulin without a potassium level can result in hypokalemia, arrythmia, and death.  Endotracheal intubation (Choice D) should be avoided in DKA whenever possible as the patient’s respiratory status serves as a compensation for the metabolic acidosis.  This patient is tachypneic and mildly confused, but he is not somnolent and does not require immediate intubation.  Intubated DKA patients need carefully monitored ventilator settings in combination with blood gas measurements to avoid worsening acidosis and cardiac arrest.  Nebulized beta-2 agonist (i.e., albuterol, salbutamol) is helpful in asthma, however this patient has DKA and not an asthma exacerbation.  IV lactated ringers solution (Choice B) is the best next step.

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Question Of The Day #83

question of the day
~ Joseph Ciano, USA ~ Leave a comment
infero-lateral MI - 41 yo male - 1 h pain
Which of the following is the most appropriate next step in management for this patient’s condition?
  • A) Provide supplemental oxygen
  • B) Administer 324mg aspirin
  • C) Administer sublingual nitroglycerin
  • D) CT head to evaluate weakness

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient arrives to the Emergency Department with several hours of shortness of breath, nausea, and generalized weakness.  On physical exam, the vital signs are normal, there is no tachypnea, no hypoxemia, no respiratory distress, and the lungs are clear.  Clear lungs in a patient with respiratory distress should raise concern for acute coronary syndrome, pulmonary embolism, cardiac tamponade, anemia, and metabolic acidosis.    

The 12-lead EKG provided shows an inferior ST-elevation Myocardial Infarction (STEMI).  This is demonstrated through the ST segment elevations in the inferior EKG leads (II, III, AvF) and the reciprocal changes in the lateral leads (most notably in AvL).  The presence or absence of chest pain is not provided in this question, but patients with acute coronary syndromes do not always have chest pain.  Elderly patients and women are more likely to present with non-chest pain anginal equivalents, like shortness of breath, lethargy, or nausea.  Diagnosis of acute coronary syndrome is done through a combination of a 12-lead EKG, blood troponin levels, and history and physical exam.  A STEMI is the most severe of all acute coronary syndromes and requires prompt recognition and treatment with antiplatelets (i.e., aspirin plus clopidogrel or ticagrelor), heparin, pain management (morphine or nitroglycerin), and percutaneous coronary intervention (PCI).  Providing supplemental oxygen (Choice A) is not necessary as the patient has no hypoxemia and a normal lung exam.  Administration of sublingual nitroglycerin (Choice C) can help alleviate ischemic chest pain and other symptoms associated with a STEMI but is contraindicated in inferior STEMIs.  Using nitroglycerin in inferior STEMIs can result in dangerous hypotension due to cardiac preload reduction.  This patient has a STEMI, and a CT head to evaluate weakness (Choice D) will not be helpful.  In general, a detailed neurological exam assessing for motor deficits will be more valuable than a CT head to determine the etiology of a patient’s weakness.  The best next step in this case is to administer 324mg aspirin (Choice B) in this patient with a STEMI.

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Question Of The Day #82

question of the day
~ Joseph Ciano, USA ~ Leave a comment
35.3 - pulmonary congestion

Which of the following is the most likely cause of this patient’s condition?

  • A) Diabetic ketoacidosis
  • B) Congestive heart failure
  • C) Myocardial infarction
  • D) Pneumonia

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient presents to the Emergency department with 1 day of shortness of breath without chest pain, fevers, or a cough.  He has been noncompliant with his home medications for his multiple comorbid conditions.  The exam shows tachypnea, tachycardia, hypertension, a low oxygen level, pulmonary crackles, and peripheral edema.  The chest X-ray shows bilateral pulmonary congestion and infiltrates consistent with pulmonary edema.

Diabetic ketoacidosis (Choice A) can cause shortness of breath, but the severe hypertension, fluid overload on exam, and lack of hyperglycemia make DKA less likely.  Pneumonia (Choice D) can cause shortness of breath, but often has other symptoms like cough, fever, and sometimes chest pain.  It is difficult to rule out an underlying pneumonia in the presence of pulmonary edema by solely looking at the chest X-ray.  The patient’s peripheral edema, severe hypertension, and lack of cough and fever make pneumonia a less likely diagnosis responsible for that patient’s symptoms.  Myocardial infarction (Choice C) often presents with chest pain but can present with only shortness of breath.  A severe myocardial infarction with cardiogenic shock can result in acute fluid overload as seen in this patient, but hypotension would be expected.  A 12-lead EKG is required to more fully evaluate for a myocardial infarction, but the constellation of symptoms this patient has makes congestive heart failure (Choice B) the most likely diagnosis. 

Immediate initial actions for this patient should include placing the patient on a cardiac monitor, obtaining a 12-lead EKG, sitting the patient upright to assist with breathing, and providing supplemental oxygen.  Acute decompensated heart failure should be aggressively treated with Nitroglycerin to lower the blood pressure and stress on the heart (preload).  Noninvasive positive pressure ventilation (NIPPV), such as BIPAP or CPAP, is another crucial initial step to help provide oxygenation, lower the preload, and push the fluid out from the lungs.  IV diuresis to remove fluid from the body and evaluating for the underlying cause are other important steps in acute CHF management. 

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Question Of The Day #81

question of the day
~ Joseph Ciano, USA ~ Leave a comment
475.3 xray abdomen series normal chest
Which of the following is the most likely diagnosis for this patient’s condition?
  • A) Pneumothorax
  • B) Diabetic Ketoacidosis
  • C) Pulmonary Embolism
  • D) Pneumonia

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient presents to the Emergency Department with 1 day of acute onset shortness of breath with pleuritic chest pain. Her exam shows tachycardia, tachypnea, a normal glucose level, and clear lungs bilaterally.  The chest X-ray provided shows no acute abnormalities.  Pneumothorax (Choice A) can present as acute onset shortness of breath with pleuritic chest pain, but the chest X-ray shows no signs of pneumothorax.  Diabetic Ketoacidosis (Choice B) can cause shortness of breath, and this patient has a history of diabetes.  However, the patient lacks other symptoms of this condition such as hyperglycemia (often glucose >250mg/dL (13.8mmol/L)), polydipsia, polyphagia, polyuria, or vomiting.  This makes DKA an unlikely diagnosis. Pneumonia (Choice D) is also unlikely as there is no fever, no cough, and no infiltrate seen on the chest X-ray provided.  Pulmonary Embolism (Choice C) is the most likely diagnosis and the correct answer.

The most common presenting symptom in pulmonary embolism (PE) is shortness of breath.  Other symptoms seen in PE include chest pain worsened by deep inspiration, unilateral leg swelling, hemoptysis, and fever.  Risk factors for PE include immobility, recent surgery or hospitalization, trauma, or hypercoagulable states (malignancy, estrogen use, Factor V Leiden mutation, antiphospholipid syndrome).  Common signs of PE on physical examination include tachycardia (common), fever (less common), and sometimes hypotension in a massive PE causing obstructive shock.  The gold standard for PE diagnosis is CT pulmonary angiography, but D-dimer blood testing, bedside ultrasound, and other tests can be useful in PE diagnosis.  The mainstay of treatment in PE is anticoagulation.  Unfractionated heparin and low molecular weight heparin are equally effective in PE.  Surgical treatment (embolectomy) and thrombolysis (alteplase) are other treatment options fo larger PEs.

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Question Of The Day #80

question of the day
~ Joseph Ciano, USA ~ Leave a comment
753 - bradycardia
Which of the following is the most appropriate next step in management for this patient’s condition?  
  • A) IV Glucagon
  • B) IV Fluids
  • C) Immediate transvenous pacing
  • D) IV Calcium gluconate

This patient presents to the Emergency department with generalized weakness and dizziness after accidently ingesting extra diltiazem tablets 1.5 hours prior to arrival.  The exam shows bradycardia, hypotension, an elevated glucose level, and a patient without altered mental status.  The EKG shows sinus bradycardia without any conduction blocks.

This patient’s clinical presentation is likely due to diltiazem overdose.  Diltiazem is a calcium channel blocker. Calcium channel blocker medications are categorized as the dihydropyridines (nifedipine, amlodipine, nicardipine) and the non-dihydropyridines (verapamil, diltiazem).  The dihydropyridines (DHPs) cause systemic vasodilation, hypotension, and often a reflex tachycardia in overdose.  The non-DHPs act more directly on the heart with less peripheral effects and cause hypotension and bradycardia.  Calcium channel blocker overdose can mimic beta blocker overdose as both medication classes have similar effects on the body. 

The initial management of any patient who has ingested a potentially dangerous medication is the “ABCs”, also known as the primary survey.  This includes assessment and management of the airway (i.e., intubation for somnolence and aspiration risk), breathing (i.e., supplemental oxygen for hypoxia), and circulation (i.e., IV fluids, vasopressors for hypotension).  Decontamination is another consideration depending on the agent the patient has been exposed to.  An EKG should be ordered early in all toxic ingestions to evaluate for signs of cardiac toxicity, such as a prolonged QT interval or prolonged QRS interval.  Checking for other dangerous coingestants, like serum levels of salicylates and paracetamol (APAP) should be routinely done.  Specific toxic effects seen in calcium channel blocker and beta blocker overdose are outlined in the chart below.

IV Glucagon (Choice A) is useful as an adjunctive treatment in both calcium channel blocker and beta blocker overdose.  However, glucagon often causes vomiting and is not a first-line agent.  IV fluids, atropine, vasopressors, and activated charcoal should be attempted before glucagon.  Antiemetics should be considered prior to IV Glucagon administration given its side effect of nausea and vomiting.  Transvenous pacing (Choice C) and IV Calcium gluconate (Choice D) are also considered second-line treatments to try when the patient is not responding to IV fluids, atropine, or vasopressors.  The best next step in this case is to administer IV Fluids (Choice B). 

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Question Of The Day #79

question of the day
~ Joseph Ciano, USA ~ Leave a comment
Which of the following is the most appropriate next step in management?
  • A) IV physostigmine
  • B) IV norepinephrine
  • C) IV sodium bicarbonate
  • D) IV metoprolol

This patient arrives to the Emergency department with altered mental status and hypotension after ingestion of multiple pills at home.  On exam, she is hypotensive, tachycardic, confused, and has dilated pupils with dry skin.  The patient has most likely ingested amitriptyline tablets given the history provided in the question.  Amitriptyline is a tricyclic antidepressant medication.  Despite the clear history, it is very important to check levels for possible other coingestants, like paracetamol (APAP) and salicylates.

Tricyclic antidepressants (TCAs) impact many different receptors in the body, so the clinical presentation of a patient with TCA overdose can vary considerably.  Important features to remember are cardiovascular toxicity with a widened QRS and hypotension, as well as an anticholinergic toxidrome.  A 12-lead EKG should be ordered early in any case of possible overdose, and an EKG in TCA overdose is a crucial step in evaluation.  Supportive care and IV sodium bicarbonate are the mainstays of treatment for TCA overdose.  See the table below for details regarding the clinical features and treatment of these patients. 

Toxic effects of Tricyclic Antidepressant (TCA) overdose

Clinical Features

Treatment

Na-channel blockade

Cardiac arrythmias,

Wide QRS (>100msec), Prominent R wave in AvR (>3mm)

IV Sodium Bicarbonate100mEq (1-2mEq/kg),

 

Titrate to QRS <100 and/or improved hypotension

Alpha-1 adrenergic receptor blockade

Hypotension

IVF, vasopressors

Serotonin reuptake blockade

Seizures

Benzodiazepines

Muscarinic- Ach receptor blockade (Anticholinergic)

Anticholinergic toxidrome– altered mental status, delirium, hyperthermia, tachycardia, hypertension, dilated pupils, dry skin

Benzodiazepines, supportive care.

 

Avoid Physostigmine.

Histamine receptor (H1) blockade

Drowsiness, coma

Supportive care

IV Physostigmine (Choice A) can be used to treat an anticholinergic toxidrome along with supportive care and benzodiazepines.  This patient does appear to have an anticholinergic toxidrome, but there is a high suspicion for TCA overdose.  Physostigmine should be avoided in TCA overdose due to data indicating worse outcomes in TCA overdose patients who receive physostigmine.  IV Norepinephrine (Choice B) may eventually be required to manage this patient’s hypotension.  However, IV fluids and sodium bicarbonate to reverse the cardiac toxicity should be used first.  IV Metoprolol (Choice D) may help relieve the tachycardia, but it would worsen the patient’s hypotension and shock state.   The best next step is IV Sodium bicarbonate (Choice C), which is the treatment for TCA overdose.  Sodium bicarbonate prevents TCA binding to cardiac sodium channels, thereby stabilizing the heart and preventing cardiac dysrhythmias and death. Sodium bicarbonate is given as an infusion until the QRS interval shortens <100msec and the hypotension improves. 

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Question Of The Day #78

question of the day
~ Joseph Ciano, USA ~ Leave a comment
Which of the following is the most likely cause for this patient’s condition?
  • A) Paracetamol (APAP) overdose
  • B) Methanol ingestion
  • C) Fomepizole overdose
  • D) Opioid overdose

This patient presents to the Emergency department from a party with slurred speech and somnolence after drinking homemade alcohol.  On exam, his vital signs and glucose are normal, he is nonresponsive to pain, and he has a GCS of 3 (normal GCS is 15).  He is intubated due to his inability to protect his airway and risk for aspiration.  Intubation is an important first step in managing this patient.

Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  The immediate evaluation and treatment of this patient should focus on the ‘ABCs’, or any abnormality in the airway, breathing, and circulation.  Any rapidly correctable causes of altered mental status, like hypoxia, hypoglycemia, or hyperthermia, should be addressed appropriately at this stage (i.e., supplemental oxygen, intubation, IV dextrose, body cooling). 

Paracetamol (APAP) overdose (Choice A) is often accompanied with little to no symptoms in the first 24hours.  Later in the ingestion timeline, liver failure and its associated sequalae can occur if no antidote is given.  The symptoms exhibited by the patient do not correlate with APAP overdose.  Opioid overdose (Choice D) can cause severely depressed mental status as seen in this patient.  However, opioid overdose also has decreased respiratory rate, pinpoint pupils, and sometimes associated bradycardia or hypotension.  This patient has normal vital signs and normal pupil size.  This patient ingested some type of alcohol at the party, but it is unclear if it is ethanol or a toxic alcohol (i.e., methanol, ethylene glycol).  Both ethanol and methanol ingestion (Choice B) can cause similar exam findings of depressed mental status as in this patient.  Other features of toxic alcohol ingestion include vision changes (methanol), hemorrhagic gastritis (isopropyl alcohol), coma, seizures, and hyperventilation (respiratory compensation for severe acidosis).  Ethanol and many of the toxic alcohols will cause an increased anion gap metabolic acidosis with an increased osmolar gap.  Helpful tests to differentiate ethanol from a toxic alcohol are serum levels of ethanol and serum toxic alcohol levels (if available).  A somnolent, intoxicated-appearing patient with a negative ethanol level should raise suspicion for toxic alcohol poisoning.  Urine studies may also show oxalate crystals in ethylene glycol ingestion. 

Since ethanol is not a listed choice and laboratory studies are not provided, methanol ingestion (Choice B) is the most likely cause of this patient’s symptoms.  Fomepizole (Choice C) is an intravenous medication that inhibits the alcohol dehydrogenase enzyme.  Fomepizole is the antidote to toxic alcohols by slowing the production of dangerous toxic alcohol metabolites.  The correct answer is Choice B.

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Question Of The Day #77

question of the day
~ Joseph Ciano, USA ~ Leave a comment

 

Test Value

Reference Range

pH

7.55

(7.35-7.45)

pCO2

20

(35-45)

pO2

84

(80-100)

HCO3

18

(22-26)

Which of the following is the most appropriate next step in management?

  • A) PO Activated Charcoal
  • B) IM Glucagon 1mg
  • C) IV Atropine 2mg
  • D) IV NaHCO3 infusion

This patient presents to the Emergency department for altered mental status, nausea, and tinnitus (ear ringing).  Her exam shows a confused female with tachypnea, tachycardia, borderline fever, wet skin, and normal pupil size.  Altered mental status has a broad differential diagnosis, including intracranial bleeding, stroke, post-ictal state, hypoglycemia, electrolyte abnormalities, other metabolic causes, infectious etiologies, toxicological causes, and many other conditions.  The immediate evaluation and treatment of this patient should focus on the ‘ABCs’, or an abnormality in the airway, breathing, and circulation.  Any rapidly correctable causes of altered mental status, like hypoxia, hypoglycemia, hyperthermia, should be addressed appropriately at this stage (i.e., supplemental oxygen, IV dextrose, body cooling).

This patient’s exam mimics many aspects of a sympathomimetic toxidrome, however, having the awareness that oil of wintergreen is a potent salicylate will lead to the diagnosis.  This patient has salicylate poisoning.  Salicylates are present in many over the counter pain medications, including aspirin, oil of wintergreen (methyl salicylate), and Pepto-Bismol (bismuth subsalicylate).   An acute overdose of salicylates may present as tachycardia, hypertension, and hyperthermia, similar to a sympathomimetic toxidrome.  Other features include tinnitus, altered mental status, seizures, and coma. 

The patient’s ABG shows a respiratory alkalosis (elevated pH, low pCO2) mixed with a metabolic acidosis (low HCO3).  Salicylic acid disrupts the body’s ability to process energy at the cellular level by acting as an ‘uncoupler’ of the oxidative phosphorylation process.  Salicylates directly stimulate the respiratory centers in the brainstem, triggering hyperventilation and increased lactic and pyruvic acid.  Hyperventilation causes the initial respiratory alkalosis, and the elevated lactic and pyruvic acid later causes an increased anion gap metabolic acidosis or a mixed metabolic acidosis and respiratory alkalosis.   

The treatment of salicylate overdose is prompt IV NaHCO3 infusion (Choice D) to alkalinize the urine and blood.  This assists in the more rapid clearance of salicylates.  Hemodialysis can be considered if salicylate levels are over 80-100mg/dL, or if there is persistent altered mental status, acidosis, or organ failure despite starting the NaHCO3 infusion.  PO Activated charcoal (Choice A) is helpful in binding certain toxins and preventing their absorption through the GI tract.  Charcoal is most beneficial when it is used early after drug ingestion.  This patient was exposed to salicylates by a topical route, so PO charcoal would not be helpful.  IM Glucagon (Choice B) is helpful in hypoglycemia and betablocker overdose.  This patient is not hypoglycemic and was not exposed to betablockers.  IV Atropine (Choice C) is helpful in patients with a cholinergic toxidrome (i.e., organophosphates, nerve gases), but would not be helpful in this patient.  Atropine would likely worsen the patient’s tachycardia.  The best next step would be IV NaHCO3 infusion (Choice D).

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