A 50-year-old female with a history of atopic dermatitis and coronary artery disease on beta blockade presents to the emergency department with shortness of breath and hives. She is on vacation and was staying at a horse farm. Along with her shortness of breath, she reports an itchy feeling in the back of her throat, sneezing, and swelling around her lips and eyes. On physical examination, she is noted to have a blood pressure of 90/55 mm Hg, an RR of 32, and a heart rate of 110 and is afebrile. Her oropharyngeal examination is notable for tongue and lip swelling and some pooling of secretions at the back of her mouth. Her cardiac examination is notable for sinus tachycardia, and her pulmonary examination is notable for bilateral wheezes. IM epinephrine is given on the mid-outer thigh. After 5 minutes, the patient demonstrates no improvement in her symptoms and she is intubated for airway protection. Repeat IM epinephrine is given. Her repeat vitals demonstrate a blood pressure of 80/50 mm Hg and a heart rate of 115. Normal saline is hung and started via a peripheral IV.
What next step could assist with the patient’s hypotension?
Correct Answer: D
Epinephrine acts on both beta-1 receptors in the heart, beta-2 receptors within the smooth muscle, and alpha-1 receptors to increase peripheral vascular resistance. For patients who are on nonselective beta blockade, the effect of epinephrine could be diminished. Glucagon should be considered in patients on beta blockers who fail to respond to the initial doses of epinephrine. Glucagon has demonstrated a positive inotropic and chronotropic effect on the heart. Unlike epinephrine, glucagon does not work through the alpha or beta receptor pathway. Glucagon works via adenylyl cyclase stimulation and cyclic AMP-dependent phosphorylation of calcium channels which enhances inotropy. Glucagon is typically given in 1 to 5 mg IV doses over 5 minutes and followed by an infusion of 5 to 15 µg/min. The main side effect to be aware of with glucagon administration is vomiting. Histamines in the form of diphenhydramine have not been associated with the resolution of hypotension. Histamine medication is used to relieve the discomfort related to skin rash and can take up to 30 minutes to work. Similarly glucocorticoids are not associated with an increase in blood pressure. They can be used to prevent or lower the risk for a biphasic reaction in the setting of anaphylaxis as they can take numerous hours to have a full effect. Finally, bronchodilators help with airway resistance but do not improve the symptoms of shock related to anaphylaxis.
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A 35-year-old male with a history of moderate persistent asthma presents to the emergency department with complaints of shortness of breath and increased wheezing. His initial vitals were notable for:
On examination, the patient was noted to be in moderate distress with increased respiratory muscle use. He did not have evidence of stridor; his pulmonary examination was notable for bilaterally wheezing and cardiac examinmation notable for sinus tachycardia. His chest x-ray demonstrated hyperinflation with flattening of the diaphragms bilaterally with no clear infiltrate. In the emergency department, he was started on IV steroids and continuous albuterol nebulizers and placed on 3 L/min of oxygen via nasal cannula. His initial basic metabolic panel was unremarkable with an anion gap of 10. An arterial blood gas showed:
On arrival to the ICU, he continues to be in respiratory distress with accessory muscle use. A repeat basic metabolic panel is performed with labs notable for a creatinine of 0.80 and an anion gap of 24; lactate level was 8. A repeat arterial gas was performed and showed :
What would be the next step in management?
Correct Answer: C
In asthmatic patients, two types of lactic acidosis can be present. Type A lactic acidosis can be seen in hypoxia as well as hypoperfusion. Type B lactic acidosis is typically seen in the setting of medication or errors of metabolism and is a result of increased lactate production or a decrease in lactate clearance. In asthmatic patients, type A lactic acidosis can be generated by multiple mechanisms. As the lung becomes hyperinflated, alveolar pressures can exceed pulmonary vascular pressures (increased West zone 1) leading to a situation where the alveolar pressure is increasingly the determinant of right-sided heart afterload. With greater afterload, there can be pressure overload of the RV and a reduction in cardiac output leading to impaired tissue perfusion. Elevated airway pressures at the end of expiration (intrinsic PEEP) also present an increased inspiratory load to the respiratory system. This requires large pleural pressure swings in order to initiate inspiration. The increase in muscle work can increase oxygen demands. The end result of either of these processes is type A lactic acidosis. Type B lactic acidosis has also been associated with asthma patients in the setting of albuterol use. Albuterol has been linked with an increase in glycolysis leading to enhanced pyruvate production which is converted to lactate. Albuterol has also been associated with increased lipolysis and production of free fatty acid. Fatty acid production inhibits pyruvate dehydrogenase which is the key cofactor needed for pyruvate to enter the Krebs cycle rather than be converted to lactate. While status asthmaticus patients can have two forms of lactate production, this patient had evidence of peak flows that were continuing to drop, evidence of pulsus paradoxus, and continued respiratory distress; therefore, type A lactic acidosis was the most likely driver. To combat the patient’s high work of breathing, it would be recommended to intubate the patient to allow for rest and better control of the patient’s ventilation. Magnesium can be used in asthmatic patients. Magnesium has been proposed to help enhance bronchial smooth muscle relaxation and enhance the receptor affinity for beta-2 agonists. It has not been demonstrated to reduce lactate production and, given the patient’s compromised hemodynamics, should not be the next best step in management. Fluids can be helpful for hypotension secondary to low-flow states. The patient may benefit from the addition of IV fluids; however, without addressing the patient’s respiratory distress, resolution of the lactate will be less likely.
A 50-year-old male with a history of obesity (BMI 35), type 2 diabetes, and GERD, who is status post right knee replacement 1 year prior, presented to the emergency room with complaints of right knee pain. His initial vitals are notable for:
His labs were notable for an elevated white blood cell count of 16 000 and a lactate of 3.0. He had a chest x- ray with no cardiopulmonary process noted. On examination, his right knee was noted to be erythematous and he was unable to flex is knee or extend his knee and was taken to the OR for concern for joint infection. Upon LMA removal at the end of the case, he was noted to be in distress with a respiratory rate of 35 with accompanying loud upper airway sounds concerning for stridor. His oxygenation saturations decreased to 83%, and given his hypoxemia and increased respiratory effort, the decision was made to reintubate the patient. A chest x-ray was performed demonstrating bilateral perihilar infiltrates.
What was the most likely cause for the patient’s respiratory distress status post extubation?
Negative pressure pulmonary edema (NPPE) occurs when significant negative intrathoracic pressures occur against a closed airway. In this case, the patient experiences laryngospasm after recent exposure to operative procedure. As the patient generates highly negative intrapleural and alveolar pressures in an attempt to overcome the upper airway obstruction, a pressure gradient is created and fluid moves out of the pulmonary capillaries and into the interstitial and alveolar spaces. The negative intrathoracic pressure also results in an increase in venous blood to the right side of the heart. This causes right-sided dilation and interventricular septum shift to the left. This reduces the stroke volume and cardiac output generated by the left ventricle. The increased venous return to the right side of the heart also increased the blood flow through the pulmonary vasculature. The increased blood increases hydrostatic forces within the pulmonary vasculature and creates a gradient in which fluid then leaks into the alveolar space. This phenomenon can be made worse as the patient becomes either more hypoxemic or acidic, as this will increase pulmonary vascular resistance which can further dilate the right side of the heart. This patient was at increased risk for laryngospasm, given he was a male and had GERD and an LMA was used which has higher rates of spasm in comparison to endotracheal tube intubation. Other risk factors for NPPE included upper airway infection, tumor, foreign body aspiration, or extended periods of time where a patient is biting down on the endotracheal tube.
NPPE can appear at times similar to cardiogenic pulmonary edema and can respond to similar treatment in the form of positive pressure and diuretics. NPPE distribution on imaging, however, can differ from cardiogenic pulmonary edema in the fact that it tends to form in the central and nondependent areas in the lungs. In these regions, a greater negative pressure is created when significant inspiratory effort is generated; therefore, these areas tend to form ground glass changes first. Cardiogenic pulmonary edema tends to favor dependent and peripheral regions.
Aspiration pneumonitis can cause acute respiratory distress; however, there is no clear history of an aspiration event. Anaphylaxis can present with bronchospasm and hypotension and can have pulmonary infiltrates. The patient did not have evidence of rash, urticaria, or swelling which can also be seen in anaphylaxis. The patient also had a clear distress that occurred after airway obstruction; therefore, the clinical picture is more aligned with NPPE. Finally, cardiogenic pulmonary edema is a very common cause of respiratory distress but does not typically follow laryngospasm.
A 40-year-old female presents to the ED via EMS after being rescued from a house fire. Upon presentation, the patient has:
The patient complains of a headache, pain on her face secondary to burn, and a hoarse voice. Her labs are notable for a carboxyhemoglobin level of 15%. On physical examination, she has a deep partial-thickness burn on the right side of her face extending from below her zygomatic arch to her jawline. She has soot in her nostrils bilaterally. She was placed on 100% oxygen.
Correct Answer: B
The patient presents with evidence of smoke inhalation injury secondary to a house fire. She has multiple risk factors for increased risk of inhalation injury which include history of inhalation in a closed space, facial burn, evidence of soot in her nasal cavity, and hoarseness. Approximately 10% to 20% of burns are associated with inhalation injury, and inhalation injury is an independent predictor of mortality. In patients with concern for inhalation injury, the greatest concern is for increasing swelling and inflammatory response which will lead to airway compromise. The mechanisms for inhalation injury include thermal injury to the upper airway, chemical irritation by combustion products which generate free radicals, damage to parenchymal tissue, and increased levels of carbon monoxide which displaces oxygen from hemoglobin and impairs mitochondrial function. Given that the patient presents with evidence of inhalation injury, after providing oxygen, a fiberoptic flexible bronchoscopy would be recommended to assess the degree of airway damage. An Abbreviated Injury Score has been created which grades the degree of injury seen on bronchoscopy by the amount of erythema, carbonaceous material, obstruction, and necrosis noted within the airway. The grading is on a 0 to 4 scale, with grades 2 to 4 on initial bronchoscopy demonstrating higher mortality in comparison to grade 0 to 1. In patients with higher grade injury seen on bronchoscopy, the decision may be made to electively intubate the patient as they are at higher risk for airway compromise.
This patient has multiple high-risk factors for airway compromise; therefore, the ideal situation would be to evaluate the airway with bronchoscopy rather than to solely observe the patient for 24 hours. If the patient were to have significant more swelling, an endotracheal tube may not be able to be passed in the coming hours and therefore an emergent tracheostomy may need to be performed. This patient also has evidence of elevated carboxyhemoglobin levels. The patient does not have a clear indication for hyperbaric chamber as her levels are less than 25; she has no evidence of ECG changes or end-organ dysfunction; and she did not have loss of consciousness. At this time, the initial therapy would be 100% oxygen. Finally, there has been no clear benefit demonstrated for steroids in inhalation injury. Steroids could potentially delay healing and increase infection risk.
A 40-year-old male with history of obesity (BMI 40) and substance abuse disorder was brought into the ED status post cardiac arrest from opioid overdose. Return of spontaneous circulation was achieved after 3 rounds of CPR and epinephrine prior to arrival to the ED. He was intubated and transferred to the ICU for further management. One week into his ICU admission, his neurologic status remained poor, and after discussion with family, the decision was made to pursue tracheostomy and PEG tube placement. He was taken to the OR for the placement of a Shiley 8 tracheostomy tube and was sedated for the procedure. Twelve hours following the tracheostomy placement, he was switched from volume control ventilation to spontaneous ventilation with an inspiratory pressure of 8 and PEEP of 10. He was noted to have increased tachypnea, and his heart rate increased to 120. The ventilator started to alert high pressures with PIPs of 40 cm H2O with each respiratory effort.
What step could prevent the high pressures?
The patient is demonstrating posterior trachea membrane occlusion status post tracheostomy placement. As the patient is transitioned to spontaneous mode of ventilation, he is able to generate his own inspiratory effort. In patients with a malpositioned or incorrectly sized tracheostomy tube, a significant inspiratory effort can cause the posterior membrane to collapse in on the distal end of the tracheostomy tube blocking air from entering. The occlusion will be seen on the ventilator in the form of high PIPs. The collapse of the posterior membrane can be diagnosed with bronchoscopy. Once the diagnosis is made, the tracheostomy tube can be replaced with a longer tube that may bypass the area of collapse, a tube with a different angle, or a tube that has a different shaft length. A T-piece tube would likely worsen the issue as there is no angle; therefore, the posterior membrane would directly be affected with each respiratory effort. If the tube cannot be exchanged quickly, the collapse of the posterior membrane may be reduced by increasing the PEEP rather than decreasing. Finally, suctioning is always recommended but is unlikely to correct the etiology for this patient’s respiratory distress.
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