- Author: Julianna Jung, MD, Johns Hopkins Medical School
- Last Update: 2015
At long last, you’ve sat down to catch up on charts for the patients you’ve seen in the past few hours. How many were there? Seven? Nine? You rummage in the pockets of your white coat – there used to be a list in there somewhere. Suddenly, the PA system blares, “MEDICAL PATIENT TO CRITICAL CARE!! ETA FOUR MINUTES!”
You’re on your feet before you’ve fully realized what’s happening, bolting for the resuscitation area. What will it be? Myocardial infarction? Sepsis? Respiratory distress? Status epilepticus? You pass the charge nurse and give her an inquiring look, but he just shrugs. Whatever it is, it will be a surprise. It’s your first night as team leader for medical resuscitations – you hope you’re ready…
By the end of the session, you will be able to:
- Describe elements of the primary survey of a critically ill or injured patient
- List signs and symptoms of airway compromise, and indications for definitive airway management
- List signs and symptoms of respiratory distress and failure
- Describe stabilizing measures for patients with respiratory distress
- List signs and symptoms of shock
- Describe stabilizing measures for patients with shock
- Explain how shock treatment differs based on etiology
What do you do before the patient arrives?
Thanks to all those miles on the treadmill, you’ve beaten the patient to the resuscitation area! How can you best prepare your team and your room?
Personnel: It is essential for every member of the resuscitation team to have a clearly defined role. The team leader is responsible for oversight of the entire resuscitation, and ideally should never touch the patient. When the leader gets bogged down in individual tasks, she loses track of the big picture, so she should delegate tasks whenever possible. Tasks to delegate include:
- Primary/secondary survey
- Airway management
- Vascular access
- Medication administration
- For cardiac arrest, establish a rotation of CPR providers and designate a quality CPR monitor whenever possible
Equipment: When a patient is really sick, say “OMI.” OMI stands for oxygen, monitor, and IV – these interventions are appropriate for every critically ill patient regardless of the cause.
- Oxygen: Be sure you have an oxygen source and a means of oxygen delivery. A cannula or face mask is appropriate if the patient is breathing, but also make sure you have a working bag-valve-mask device in case the patient is apneic. If time permits, set up intubation equipment as well.
- Monitor: Set up a cardiac monitor and pulse oximeter, and make sure that you have a working defibrillator in case of serious dysrhythmia.
- IV: Set up equipment for establishing peripheral IV access. If time permits, set up advanced vascular access equipment as well – intraosseous and/or central central line kits.
The patient is here…now what?
You know you need to conduct a primary survey, but where to begin? Is it really as easy as A-B-C? Or is it C-A-B now? Why did they have to go and change it? Where should you start?
ABC versus CAB
In short, ABC is for the living and CAB is for the dead. The goal of the CAB assessment, which is the standard of care in cardiac arrest, is to rapidly determine whether to initiate CPR. If your patient is moving, talking, moaning, breathing, or otherwise demonstrating obvious signs of life, they may have 99 problems, but cardiac arrest isn’t one of them! These patients do not need CPR, and can be assessed in ABC order.
If your patient does not exhibit signs of life, you should assume that they are in cardiac arrest until proven otherwise, and conduct a CAB assessment. The CAB assessment consists of palpating the carotid pulse for less than ten seconds while simultaneously observing for respiratory effort. If at the end of ten seconds you are not 100% certain that the patient has a pulse, start CPR. You are very unlikely to injure a patient significantly by performing unnecessary CPR, whereas withholding needed CPR virtually guarantees your patient’s death. So when in doubt, start CPR!
Your patient is moving and moaning, but he doesn’t look so good. In any case, you know that he doesn’t need CPR, so you plan to conduct your primary survey in ABC order. Here goes…
The Primary Survey
The goals of the primary survey for critically ill patients are twofold:
- Rapidly and systematically identify life threats
- Provide simultaneous treatment of all life threats identified
This means that the primary survey isn’t just about assessment. It’s about synthesizing the information gained during the assessment in order to recognize imminent life threats, and providing immediate stabilization for life threats. You should never proceed with assessment when you identify a life threat during the primary survey – you should stop and deal with each threat as you identify it. For this reason, assessment and treatment topics will be interspersed throughout the discussion below.
You approach the bedside, place your hand on the patient’s shoulder, and introduce yourself. “Get off me!” your patient growls. You smile and announce, “Airway’s intact!”
The ability to speak is the single most important indicator of airway patency. By definition, any patient who is able to phonate has an intact airway…for now.
When your patient is unable to speak, you must immediately determine why, and assume that they have the potential for serious airway compromise until proven otherwise. Not every patient who is unable to speak will have a compromised airway – conditions that alter mental status or language function may prevent speech without affecting the airway. However, the burden is on you to demonstrate that these patients have and are able to maintain patent airways.
There are many signs on rapid physical examination that may suggest a compromised airway.
- Look – Externally examine for swelling of tongue, lips, or neck. Look inside the mouth for foreign bodies, loose teeth, vomitus or secretions. A word of caution – look but don’t touch! Blind finger sweeps are more likely to worsen than alleviate airway obstruction.
- Listen – Noisy breathing is obstructed breathing, so listen with the naked ear to the sound of respiration. Snoring or gurgling are signs of mild-moderate upper airway obstruction, usually with soft tissue or secretions. Stridor, a high-pitched inspiratory sound, suggests high-grade upper airway obstruction – this is always an emergency.
- Feel – Palpate the neck and upper chest for crepitus, which can be a sign of pneumothorax or tracheolaryngeal injury. Feel for swelling or masses in the neck as well, as these may lead to airway compromise in the future, even if the airway is patent now.
Even if there is no sign of immediate airway compromise, consider the likelihood that the airway will become obstructed in the near future. A patient with angioedema, for example, may have no significant airway compromise on presentation, but 30 minutes later can develop complete obstruction. The time to intubate is before the patient loses their airway!
Some conditions that can lead to progressive airway compromise:
- Foreign body aspiration
- Retropharyngeal abscess
- Ludwig’s angina
- Bacterial tracheitis
- Neck mass/hematoma
- Facial fractures
Man, you sure are glad that this guy’s airway is okay! But what would you do if it wasn’t? What if he was stridorous, or unable to speak?
The first question to be answered in airway management is whether your patient needs to be intubated. Not every patient with compromised airway or breathing requires intubation. Many patients with snoring or gurgling respirations can be managed conservatively, with positioning or nasopharyngeal airway placement. Many patients with hypoxia can be stabilized with supplemental oxygen or respiratory therapies. The following are indications for intubation:
- High-grade airway obstruction of any etiology
- Suspected imminent airway obstruction of any etiology
- Inability to maintain or protect the airway over time
- Severe hypoxia refractory to less invasive treatment
- Severe hypercarbia refractory to less invasive treatment
The next critical aspect of airway management is deciding when and by whom intubation should be performed. The key to making this decision safely is recognizing a potentially difficult airway and planning management strategies accordingly.
Any condition that distorts the normal anatomy of the face and neck, whether congenital or acquired, will make intubation difficult. “LEMON” is a helpful mnemonic for remembering signs of a potentially difficult airway:
- Look: visual inspection of the face and neck can reveal anatomic or cosmetic factors that make intubation difficult: facial dysmporphism (particularly micrognathia), obesity, dental abnormalities, short or thick neck, facial/neck trauma or swelling
- Evaluate 3/3/2: this rule refers to the normal facial and neck anatomy in terms of the patient’s finger breadths – if any of these measurements are less than the amount specified, expect trouble:
- 3 finger breadths between the incisors when the mouth is opened
- 3 finger breadths from the mental vertex to the hyoid bone
- 2 finger breadths from the hyoid bone to the thyroid notch
- Mallimpati: this is a great tool for cooperative patients in the preoperative setting, but is less useful for critically ill patients in the ED. It requires that the patient sit upright and voluntarily open the mouth as widely as possible. The score is based on how much of the posterior pharynx can be visualized.
- Obstruction: check for foreign body, listen for stridor as above
- Neck mobility: assess range of motion of the neck, as limitations can make positioning for intubation difficult. Note that trauma patients have limited neck mobility by definition, as they are typically immobilized for protection of the cervical spine, though this does not usually present a significant obstacle to airway management.
When a difficult airway is anticipated, first and foremost, GET HELP. Most hospitals have some sort of difficult airway response team, and this team should be activated immediately when a difficult airway is anticipated. For patients with difficult airways, it is essential to expect that standard intubation will fail, and to prepare backup plans including surgical cricothyrotomy. Patients with difficult airways should never receive sedative or paralytic agents until all necessary equipment and personnel required to implement backup plans for a failed airway are present and available.
Okay, the airway is good. What’s next? B – breathing! Well he IS breathing, that’s a start – but is he breathing adequately? How do you decide?
The first and most important question is indeed whether your patient is breathing! If your patient is apneic, this is an emergency and requires immediate intervention in the form of assisted ventilation.
Assuming your patient is breathing, the next step is to determine whether their breathing is adequate and likely to remain that way. Important examination steps include:
- Look: Assess the patient’s respiratory effort – are they breathing slowly or quickly? Deeply or shallowly? Using accessory muscles? Sitting up in the “tripod” position? More importantly, develop your gestalt sense of the patient’s work of breathing – does it look easy or effortful? Remember that normal respiration is almost imperceptible, so anytime you can really see a patient breathing, their work of breathing is increased.
- Listen: Don’t worry about the subtleties of auscultation – the critical care room is no place for whispered pectorliloquy! Listen to make sure that there are breath sounds –a lot of respiratory effort that produces minimal air exchange is a sign of imminent respiratory failure. Then make sure you hear breath sounds on both sides – unilaterally absent breath sounds may suggest a tension pneumothorax, which requires immediate treatment. Finally the quality of the breath sounds may provide a clue as to the underlying diagnosis.
- Count: There is no substitute for a respiratory rate that you count yourself. Documented respiratory rates are commonly inaccurate, and this is an critical vital sign for a patient in respiratory distress.
- Monitor: The oxygen saturation is really the “bottom line” on respiration, at least in the short term. The whole mission of the lungs is to deliver oxygen to hemoglobin, which will in turn deliver it to organs and tissues. If the oxygen saturation is low, some significant pathology is present which is causing the lungs to fail in their mission. Anything less than 96% is abnormal, and anything less than 90% is potentially life-threatening.
The goal of your respiratory assessment is to determine whether your patient has respiratory distress or failure. Patients with respiratory distress are attempting to compensate for underlying pathology that has deranged their pulmonary function. Generally patients with respiratory distress are successfully compensating to some extent, meaning that their increased effort is effectively improving their oxygenation and/or ventilation. The problem is that this is very metabolically demanding, and patients can’t maintain this degree of effort indefinitely. This means that patients with severe distress that is not alleviated will progress to respiratory failure. These patients are exhausted, and no longer able to compensate for their underlying pathology.
|Respiratory Effort||Breath Sounds||Oxygen Saturation||Carbon Dioxide Level|
|Normal-Minimal Distress||Normal/slightly increased||Good air movement||Normal/slightly decreased||Normal|
|Moderate-Severe Distress||Markedly increased||Often decreased||Moderately decreased||Normal/slightly decreased|
|Failure||Normal/ decreased||Often decreased||Markedly decreased||Increased|
Okay, this guy’s pretty tachypneic, and you can definitely see that he’s working hard. This is pretty bad respiratory distress – you’d better do something! But what?
Management of Respiratory Problems
Apnea and Agonal Respirations
Again, the first priority is to make sure your patient IS breathing, and to provide assisted ventilations if not. Assisted ventilations are given using a bag-valve-mask (BVM) device, attached to 10-15L/min of oxygen. BVM ventilation is ONLY performed on patients with agonal or absent respirations. Do not attempt to perform BVM ventilation on a spontaneously breathing patient – this is poorly tolerated and tends to worsen hypoxia.
The goal of assisted ventilations is to produce visible chest rise. If ventilation is ineffective (i.e., no chest rise is observed), then troubleshoot your technique:
- Optimize patient position: Is the patient lying flat, with no pillows or clothing in the way? Is the patient in the “sniffing position,” with the neck slightly flexed and the head slightly extended? Sometimes a shoulder roll is needed to achieve this position, as the occipit tends to force the head into flexion.
- Optimize your position: Are you standing squarely at the head of the bed? It is not possible to correctly perform BVM ventilation from the side. Are you holding the mask to the face using the “C/E” technique?
- Use two-person technique: Sometimes even with perfect positioning, it isn’t possible to perform effective BVM ventilation. When this occurs, the person managing the airway can use two hands to hold the mask to the face, while an assistant squeezes the bag to provide breaths. This is much easier and more effective than single-person technique, particularly for large patients and/or small providers.
- Use an oropharyngeal airway: This device hooks over the root of the tongue, pulling it forward out of the hypopharynx. It is so helpful for maintaining airway patency during BVM ventilation that it should feel wrong to use a BVM device without one!
The vast majority of patients can be effectively ventilated with proper BVM technique. Patients don’t die from not being intubated, they die from not being ventilated – meaning that if you are able to effectively ventilate using a BVM device, there is no urgent need for intubation. You may ultimately intubate the patient if indicated, but in the initial phase of resuscitation, BVM is perfectly acceptable provided it produces adequate chest rise.
Every patient with respiratory distress should receive some form of oxygen therapy. Oxygen delivery options include:
|Nasal Cannula||1-6L/min||<30%||Mild distress/ hypoxia|
|Venturi Mask||Variable||24-50%||Moderate distress/ hypoxia|
|Nonrebreather Mask||10-15L/min||Up to 90%||Severe distress/ hypoxia|
|BVM Device||10-15L/min||Nearly 100%||Apnea|
Oxygen therapy is initially appropriate for every patient with respiratory distress. However, prolonged use of oxygen can be detrimental, particularly at high concentrations, so be sure to titrate oxygen to the lowest flow rate appropriate for your patient.
Noninvasive positive pressure ventilation (NIPPV) is a helpful treatment for some common causes of respiratory distress, including pulmonary edema, asthma, and chronic obstructive pulmonary disease (COPD). Modes of NIPPV include continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP). Physiologic benefits of NIPPV include improved oxygenation, reduction in work of breathing, recruitment of collapsed alveoli, and redistribution of fluid from alveoli back into the vasculature. NIPPV has been shown to reduce need for intubation for patients with COPD and pulmonary edema, and is considered the standard of care for moderate-severe cases of these conditions. NIPPV requires use of a tight-fitting mask, which is poorly tolerated by some patients, and it is absolutely contraindicated in patients who are unable to maintain or protect their airways.
Other treatments for respiratory distress are disease-specific. There is a broad differential diagnosis for respiratory distress, including pulmonary, cardiac, neurologic, and metabolic conditions. Clues to the underlying cause of respiratory distress can be obtained through history, physical examination, and ancillary tests like chest imaging and laboratory studies. All patients with significant respiratory distress should be auscultated to ensure that bilateral breath sounds are present, as tension pneumothorax must be identified and immediately treated if present. All patients should also undergo chest radiography to screen for common causes of respiratory distress. Further workup should be guided by clinical suspicion.
The goal of treating respiratory distress is to prevent progression to respiratory failure. Despite treatment, some patients will progress to respiratory failure, and it is important to recognize and promptly manage these patients. Patients in respiratory failure are no longer able to compensate for their underlying disease process, and require respiratory support. In some cases this can be accomplished with NIPPV, but usually intubation and mechanical ventilation will be required. Treatment directed at the underlying cause of respiratory failure should always be provided along with respiratory support.
Some important causes of respiratory distress and failure:
|Diagnosis||Immediate Stabilization||Definitive Treatment|
|Tension Pneumothorax||H&P||Needle decompression||Tube thoracostomy|
|Asthma/COPD||H&P, CXR||O2, NIPPV||Bronchodilators, steroids|
|Pulmonary edema||H&P, CXR, pro-BNP||O2, NIPPV||Nitrates, diuretics|
|Pulmonary embolism||H&P, d-dimer, chest CT||O2||Anticoagulation, thrombolysis (massive PE only)|
|Acute respiratory distress syndrome||H&P, CXR||O2, NIPPV||Ventilatory support|
|Myocardial infarction||H&P, EKG||O2, nitrates, aspirin, anticoagulation||Revascularization (thrombolysis or PCI)|
|Metabolic acidosis||H&P, metabolic panel, blood gas||O2||Directed at underlying cause|
Well, your patient is breathing a little better with some oxygen going, but now that he’s on the monitor you see that he’s really tachycardic, and his blood pressure is pretty low. Oh crap – is he in shock? What should you do to figure it out?
The goal of circulation assessment is to figure out if your patient is in shock. Shock is a physiologic state characterized by inadequate delivery of oxygen to meet metabolic demands at the tissue level. Shock can’t be seen or measured directly, but there are signs and symptoms that can provide clues about whether shock is present.
- Heart rate: Tachycardia is one of the first compensatory responses to shock. Hypoperfusion elicits a sympathetic nervous system response, increasing heart rate and contractility in order to raise cardiac output. Remember that tachycardia may not always be present, especially in patients with underlying cardiac disease or medications that lower the heart rate.
- Pulse pressure: The sympathetic response to hypoperfusion also leads to vasoconstriction, raising the diastolic pulse pressure. In compensated shock, the systolic pressure will remain normal, while the diastolic increases, leading to a decrease in pulse pressure. Again, this phenomenon may not be observed in patients with vascular disease or those using vasodilating medications.
- Respiratory rate: Remember, shock is a disease of tissue-level hypoxemia, so the body will raise the respiratory rate in an effort to provide additional oxygen to the tissues. Tachypnea is common in shock, and does not necessarily imply a pulmonary etiology of shock.
- Blood pressure: Hypotension is a sign of uncompensated shock, and occurs when compensatory mechanisms are no longer adequate to support perfusion. It is important to remember that hypotension is a late sign of shock, and shock may be present in the absence of hypotension. It is also important to consider the patient’s baseline blood pressure – a patient who normally lives at 170 may be in shock at 110.
- Mental status: Patients with compensated shock are generally alert, though may be anxious and apprehensive. In uncompensated shock, cerebral hypoperfusion leads to confusion or decreased level of consciousness.
- Other physical exam findings: there are a variety of physical exam findings which have been suggested to correlate with volume status, though evidence for the accuracy of these in adults is quite limited. Signs to consider include:
- Skin color: pink indicates good perfusion, whereas pallor or cyanosis suggest the opposite. Look at mucous membranes (mouth, conjunctiva) in dark-complected patients.
- Capillary refill: under 2 seconds is normal, longer refill times suggest hypoperfusion.
- Skin turgor: when pinched, the skin should return to its normal configuration in less than 2 seconds – longer suggests hypoperfusion
- Pulse strength: bounding pulses suggest good perfusion, weak/thread pulses suggest the opposite
- Extremity temperature: cold extremities suggest shock, as the body shunts blood centrally to maintain vital organ perfusion
- Mucous membranes: dry membranes suggest dehydration
Causes of Shock
There are four physiologic classes of shock, and it is important to determine which one applies to your patient, as management differs between them. Causes of shock include:
- Hypovolemic: occurs when circulating blood volume is significantly reduced. Can be caused by hemorrhage (internal or external), and by GI or urinary losses of water.
- Cardiogenic: occurs when the cardiac “pump” fails. Caused by disease processes that directly affect the myocardium, impairing contraction.
- Distributive: occurs when the vasculature is abnormally dilated and/or leaky. Caused by disease processes that impair vascular tone and increase permeability, like sepsis and anaphylaxis.
- Obstructive: occurs when there is an extra-cardiac obstruction to blood flow. Caused by disease processes that impair cardiac filling, like tension pneumothorax and cardiac tamponade.
History and physical exam findings can provide helpful clues about the cause of your patient’s shock, and can allow you to select the right treatment. Bedside ultrasound is also a very helpful adjunct in evaluating the patient. The chart below summarizes diagnosis and treatment for the various causes of shock.
|History||Physical Exam||Ancillary Tests||Treatment|
|Hemorrhagic Shock||Trauma, GI bleeding, abd or back pain (ectopic/ AAA)||External bleeding, hematemesis/ hematochezia, abd/flank tenderness||FAST ultrasound (trauma/ ectopic), aortic ultrasound (AAA), hCG, CBC (Hgb)||IV volume administration (fluid followed by blood as needed), NO vasopressors|
|Hypovolemic Shock||Diarrhea, vomiting, polyuria, poor PO intake||Dry mucous membranes, decreased urine output||Blood glucose (hyperglycemia) metabolic panel, UA||IV fluids, NO vasopressors|
|Cardiogenic Shock||Chest pain, dyspnea, CHF signs, viral prodrome (myocarditis)||Elevated JVP, pulmonary crackles, pedal edema, ascites||EKG, CXR, Bedside echo to estimate ejection fraction||Vasopressors, address underlying cause|
|Septic Shock||Preceding febrile illness, sx of infection source, immuno-suppression||Fever, sx of infection source||CBC (leukocytosis), UA, CXR, +/- LP, +/- other imaging for infection source||IV fluids, antibiotics, source control, vasopressors if needed|
|Anaphylactic Shock||Allergic exposure/rash||Angioedema, urticaria||None||Epinephrine, antihistamines, IV fluids, airway control|
|Obstructive Shock||Risk factors for pulmonary embolism, pneumothorax, tamponade||Unilateral leg swelling (PE), unilaterally absent breath sounds (PTX), muffled heart sounds or JVD (tamponade)||D-dimer or chest CT (PE), FAST ultrasound (PTX), bedside echo (tamponade),||Thrombolysis (PE), decompression/ chest tube (PTX), pericardio-centesis (tamponade)|
Great, you’ve assessed your patient and he is definitely in shock but you’re not 100% clear on why – what can you do for him while you figure it out?
Management of Shock
As noted above, management of shock varies by etiology, so it is important to consider the cause of shock before beginning treatment.
Monitoring: every critically ill patient should be monitored. In shock, monitoring of heart rate and blood pressure will help you determine your patient’s degree of physiologic compromise, and keep track of their response to interventions.
Vascular access: Every patient with shock must have adequate vascular access. For an adult, this means two “large-bore” peripheral IVs (18g or bigger), or an intraosseous line, or a central line. Remember that intraosseous lines are safe and simple, and are preferred over central lines for patients who need rapid access. Also remember that central lines are long and skinny, and therefore poorly suited for large-volume resuscitation – if your patient needs a lot of fluid or blood, use peripheral or intraosseous access, or place a large-caliber “trauma line.”
IV fluids: When confronted with shock, the knee-jerk reaction of most clinicians is to give IV fluids. Although the treatment of shock varies by etiology, IV fluids are helpful (or at least not harmful) as an initial stabilizing measure in all etiologies of shock except cardiogenic. Patients with cardiogenic shock are generally volume overloaded at presentation, and IV fluid will extravasate into the lungs, worsening respiratory status. For this reason, it is important to include examination for signs of cardiogenic shock in your initial assessment, and refrain from giving fluids in these cases. In the absence of cardiogenic shock, it is appropriate to begin fluids during the assessment process. Isotonic crystalloid solutions are the fluids of choice (normal saline or lactated ringers), and they should be given in bolus form. Patients who are potentially fluid-sensitive should receive small boluses (250-500cc). and should be assessed for signs of pulmonary edema after each one.
Vasopressors: Vasopressor support is essential for the treatment of some forms of shock, but is absolutely contraindicated for others, so make sure you know what you’re dealing with before you use these drugs!
- Hypovolemic/hemorrhagic shock – do not use vasopressors! The treatment is volume, not drugs.
- Cardiogenic shock – use vasopressors to support inotropy and vascular tone. Norepinephrine is the first-line agent.
- Septic shock – start with fluids, but if inadequate response to 30cc/kg of crystalloid, then begin vasopressors. Norepinephrine is the first-line agent.
- Anaphylactic shock – epinephrine is the drug of choice in all cases, and it is not necessary to begin a fluid challenge before administering it.
- Obstructive shock – do not use vasopressors! The focus of treatment must be on alleviating the underlying obstruction.
Special Cases of Shock
Trauma: When traumatically injured patients present in shock, there is a more limited differential diagnosis, and specific treatments must be provided:
- Diagnosis: This is the cause of shock in the vast majority of trauma cases. Remember that the blood can be at the scene, on the floor in the ED, or inside a large body cavity. FAST ultrasound can help you locate the source of blood loss.
- Treatment: IV fluids can be given for initial stabilization, but refractory shock requires blood products. Most patients with hemorrhagic shock from trauma will require surgical intervention, so involve your trauma team early.
- Cardiac tamponade
- Diagnosis: This most commonly occurs with direct injuries to the heart, and can be diagnosed with FAST ultrasound.
- Treatment: Emergent pericardiocentesis, followed by a trip to the OR for a pericardial window.
- Tension pneumothorax
- Common with blunt or penetrating chest injuries. Should be diagnosed clinically (shock, hypoxia, unilaterally absent breath sounds), though can also be seen on e-FAST or CXR.
- Treatment: Emergent stabilization with needle decompression, followed by a tube thoracostomy
Coagulopathy: For obvious reasons, bleeding will always be worse in a coagulopathic patient. For all bleeding patients, be sure to ask about diseases leading to coagulopathy (hemophilia, liver failure), and about use of antiplatelet and anticoagulant medications. Coagulopathic patients with life-threatening bleeding should receive appropriate treatment to reverse their coagulopathy in order to stop bleeding. Potential treatments include blood products, medical antidotes, or clotting factor replacement, depending on the underlying cause of coagulopathy.
Okay, your patient is on oxygen, he’s on the monitor, and he’s got great IV access. You’ve started a neb treatment and some fluids, and you’ve ordered the right tests to get to the bottom of his problem. You’ve still got a way to go to get to a definitive diagnosis, but he looks a lot better already. As you’re setting up for bedside ultrasound, he looks up at you and says, “Thanks, Doc. I feel a bit better, and I know I’m in good hands with you.”