>> Understand the pathophysiology of shock and end-organ failure in medical emergencies.
>> Create a prioritized list of differential diagnoses for a patient experiencing a medical emergency.
>> Differentiate between life-threatening medical conditions and other less-dangerous conditions.
>> Incorporate point-of-care blood chemistry findings into a prehospital assessment and care.
“Medic 23,” the radio crackles, “Delta level response to the fairgrounds first aid tent, 10 Dan Patch Drive for a 55-year-old female feeling ill. Your time out is 1330 hrs.”
Acidosis: Lower than normal pH due to increased hydrogen ion concentration.
Co-morbidity: Existing simultaneously with and usually independently of another medical condition.
Differential diagnosis: A systematic method of weighing the probability that one disease or another is causing the patient’s condition.
Psychosis: Any major mental disorder with a physical or emotional source.
Shock: Inadequate perfusion to tissues and organs.
Your patient is Nadifa, a 55-year-old, 95 kg Somali female wearing a full-length dress and head scarf. On this humid August afternoon, the temperature at the state fair has reached 95° F. Nadifa was participating in a 5-mile walk event when bystanders say she began to speak incoherently and vomit, was assisted to the ground and became unconscious.
The on-site medical aid team quickly carried her to a nearby first-aid tent, where a physician’s assistant and an athletic trainer began patient care. On your arrival, Nadifa is semi-conscious and complains of diffuse abdominal pain and several episodes of emesis.
You note yellowish sputum around her mouth. Her vital signs are pulse 108, blood pressure 88/40, respiratory rate 34 breaths per minute, saturation of peripheral oxygen (SpO2) 99% on room air and tympanic temperature 100.2° F.
Her blood glucose level is 86 mg/dL. The physician assistant on scene shows you digital results of the iStat point-of-care blood test. Her lactate is 5.2 mg/dL, potassium 4.6 mEq/L and troponin 0.00 mg/dL; her teenage son tells you she’s normally healthy but has been running a fever and went to see a traditional healer yesterday.
This healer used Haba sodah massage and had Nadifa drink camel’s milk to induce urination and bowel movements. He hands you two prescription medications from Nadifa’s purse: Captopril and Metoprolol.
Caring for a patient with hypotension, abdominal pain and altered mental status (AMS) can be challenging. A thorough history and physical is needed to assess and treat this complex patient.
Gathering this information is especially challenging when the patient is unable to report their history, or speaks another language.(1) It’s lucky that a family member was available and well informed in this situation.
In this case, the challenges are multiplied by the high environmental temperature, the crowded fair venue with specialized medical services and the cross-cultural issues with traditional healing methods. Cases of this type play out every day in the real world of prehospital care. Your ability to appropriately assess and differentiate which assessment findings are useful and which to ignore is essential to good patient care.
At first glance, this would seem to be a simple case of heat exhaustion and dehydration. The outside temperature, clothing and patient’s weight might lead a novice provider to quickly jump to a diagnosis and then look for clues to confirm it. This common error in medicine is called confirmation bias.(2–4) We look only for other confirmatory findings, ignoring or omitting other assessment findings that may not fit or give us additional clues about other problems.(5)
In this case, the on-scene medical crew did a great job of checking Nadifa’s blood sugar, temperature and SpO2 level; they used point-of-care lab technology to obtain lactate, potassium and troponin levels. This greatly assists the arriving ambulance as long, as the providers can put this information together and not be overwhelmed, intimidated or misled by it.
Today’s prehospital clinicians must be able to create accurate field impressions, or working diagnoses—often with less-than-ideal information—to properly care for the patient. The EMS provider has to begin with a broad, comprehensive list of possible diagnoses, otherwise known as a “wide differential diagnosis,” because so many diseases and conditions can cause a change in mentation and hypotension.
Formulating an accurate differential diagnosis is one of the most important actions of a prehospital professional. This list of possible causes of a patient’s presentation focuses the treatment efforts, helps prioritize interventions and determines hospital disposition.
Our focus is on becoming the medical detective who solves the mystery by determining potential threats to life or limb.
This comprehensive list also helps us ensure we aren’t getting so focused on any one possibility (also called tunnel vision) that we miss another condition, which might be life threatening. The next task is to try to narrow down the comprehensive list by systematically ruling out or ruling in various possibilities.
If a problem can’t be definitively ruled out with an objective test, it must remain on the list and be treated as a real possibility until proven otherwise. As the old adage goes, it pays to be a little bit paranoid, and EMS needs to have a high index of suspicion for lethal conditions.
You can think of medical assessments in the same way a detective would think of solving a murder mystery. We gather evidence and listen to the story while making a list of possible suspects. As the stories, allibies and forensic lab tests come back, we can broaden or hopefully narrow the list of suspects. When we aren’t sure, it’s better to leave a suspect on the list than risk forgetting about them, letting them get away or worse yet, allowing them to kill again.
This suspect list is also being simultaneously prioritized. Sometimes it’s in the order of most likely suspect (perhaps a repeat offender or career criminal who just got released from jail would be most likely), but also making a list of the most lethal (an unlikely suspect who’s armed, dangerous and could easily kill again if you let your guard down). Finally, you want to keep an eye on all of your suspects, watching and addressing each.
In medical terms, your suspects are the diseases or conditions affecting your patient. In EMS, we want to discover and treat, or at least closely watch, any potentially lethal conditions before dealing with less dangerous ones.
For example, we must suspect that every patient with chest pain is having a heart attack until history, physical exam, ECG, and sometimes blood work days later, suggest otherwise. Likewise, patients with ankle injuries should be suspected of having a fracture rather than a sprain and treated with good splinting until the patient can be evaluated by a physician.
Vital signs are a key component of your data collection, and additional information can be gained by the use of other tools at your disposal, such as end-tidal carbon dioxide (EtCO2) monitors or ECGs. In one recent study, exhaled EtCO2 values of less than 21 mmHg were 84% predictive of patients who were later confirmed to be acidotic with a blood test.(6)
A good acronym to help us round up the usual suspects, or the lethal list of suspected conditions that cause AMS, is AEIOU TIPS (see Table 1, below). This broad list takes into account a wide range of problems, from metabolic derangements (e.g., shock and acidosis) to a simple case of fright (e.g., psychosis).
Table 1: AEIOU TIPS
A Alcohol, acid/base disorders, arrhythmias
E Encephalopathy, endocrine disorders, electrolyte disorders
I Insulin issues (hypo- or hyperglycemia)
O Opiates, overdose
T Trauma, tumor, thermal insult (hypothermia)
I Infection, intracerebral vascular disorders
P Poisonings, psychogenic, shock (fainting)
In Nadifa’s case we can easily rule out “T” for trauma, from the history we have; “I” (insulin/diabetic) because the blood glucose is within normal limits; and “P” for psychosis, because there are clearly some abnormal physical findings. The rest are plausible, so we need to keep these on our list of suspects and start prioritizing them.
Our history uncovered that Nadifa was taking herbal supplements that led to urination and diarrhea. She had just completed a significant exertional episode. Additionally, she had a fever before the race. With this information, we can predict that she may have had significant volume loss prior to entering the race. The past medical history revealed that she was on two anti-hypertensives: captopril, an angiotensin converting enzyme (ACE) inhibitor, and metoprolol, a beta blocker.
Using a smartphone app to look up the pharmacology of these medications reveals that ACE inhibitors can lead to renal failure in hypovolemia, and beta blockers can prevent tachycardia. Our physical exam revealed a patient whose ability to sweat was diminished due to her clothing. Vital signs showed some mild tachycardia despite her beta blocker, hypotension and increased respiratory rate.
The information you gain from your history and physical exam will be vital in determining the underlying cause of your patient’s shock. In our case, the patient has just completed a strenuous activity.
Exertion can be closely associated with both hypovolemic and cardiogenic shock. Combining objective exam findings with this history can further narrow the differentials.
Think critically about what information you need and prioritize your activities accordingly. Evaluate for signs of blunt or penetrating trauma while looking for evidence of fluid loss. Bleeding, vomit and diarrhea can all lead to hypovolemic shock. Ischemic changes on an ECG suggest a cardiogenic component, while the absence of breath sounds suggest an alternate cause.
Identification of a uticarial rash or the presence of an epinephrine pen at an unconscious patient’s side would lead you down another path.
In EMS, we aren’t used to having point-of-care laboratory values available to us. As point-of-care technology becomes more common, prehospital providers will increasingly encounter, or perhaps obtain, this data. Understanding the changes that shock causes on a biochemical scale and how these are reflected in the measured lactate and pH levels can be very helpful and even guide your treatment.
It’s also important to keep in mind that no matter what the root cause of the medical problem, all paths will lead to the same final outcome: shock.
Pathophysiology of Shock
As we evaluate patients, we must always assess for the presence of shock. By definition, shock is a state in which the global, or whole body, delivery of oxygen isn’t sufficient to meet demand. We can see this from a variety of causes, including hemorrhage, sepsis, spinal cord injury, anaphylaxis, pulmonary embolism or tension pneumothorax.
Classically, shock often initially presents with tachycardia, as the heart speeds up to compensate for initial lack of good perfusion. If heart rate alone can’t adequately compensate, then blood pressure may eventually fall and result in end-organ hypoperfusion.
But remember that by the time blood pressure falls, the patient has progressed far down the path toward decompensation. Our goal should be to identify shock early—while the patient continues to compensate. Laboratory analysis can be critical for confirming a diagnosis of early shock.
Shock may progress rapidly in patients who have one or more pre-existing conditions (also called co-morbidities). In our case, the metoprolol medication that Nadifa takes for hypertension is worsening the situation. This is a beta blocker that’s preventing the heart from speeding up and compensating for her volume depletion.
When the body enters a state of shock, the normal method of using oxygen to generate energy aerobically is no longer possible and the body switches to an anaerobic state. Anaerobic metabolism is much more inefficient, yielding just two molecules of adenosine triphosphate (ATP) (i.e., the body’s energy source) vs. 38 in an aerobic system. In the process, lactic acid is released. This process drops the pH of the blood, making it more acidic.
By directly measuring the blood lactic acid (i.e., lactate) level or by measuring pH as a proxy for acid production (pH falls as acid levels increase), we can detect the biochemical dysfunction on a cellular level before it may become apparent on our clinical exam.7–9
As the acid content of the blood increases, the patient develops progressive multi-organ dysfunction syndrome. As the brain starts to fail, the patient will develop AMS. The skin is the largest organ in the body and mottling is a sign that it’s hypoperfused. Cardiac output is negatively affected by acid (think “Hs” and “Ts” of ACLS) and contractility can decrease. Finally, renal failure will ensue, and the urine output will fall and eventually may cease. Recognizing that an elevated lactate (or a low pH) level suggests that a patient is in shock is vital, even though we may not know what kind of shock they’re in.
Clearly, the restoration of aerobic respiration is vital to ensure the body can generate the energy (ATP) needed to survive. This is accomplished by eliminating the oxygen supply/demand mismatch and ensuring adequate oxygen delivery to the tissues. For all shock patients, this means ensuring that their hemoglobin is adequately saturated with oxygen. Blood pressure management must be individualized to the type of shock your patient is suffering from.
Types of Shock
Identifying a patient as being in shock isn’t the end of diagnostic thought process, but rather the starting point to formulate your differential diagnosis. Understanding the types of shock is necessary to compile your differential diagnosis for the cause of shock in this patient.
Shock can be broken down into four major forms: hypovolemic, distributive, obstructive and cardiogenic.
Hypovolemic: A hemorrhaging patient will benefit most from stopping the blood loss by applying direct pressure or a tourniquet. Administering normal saline until you can feel a radial pulse will improve perfusion while not overly diluting the remaining hemoglobin because normal saline doesn’t carry oxygen.
Distributive: Septic and anaphylactic patients go into shock because their blood vessels have lost their muscular tone and dilated out, effectively increasing the size of their vascular space. These patients haven’t lost any blood (if hemoglobin levels are normal) but require several liters of fluid to fill up the additional volume.
Obstructive: This form of shock involves a physical obstruction to a large vessel or the heart itself. This type of shock needs to be reversed by removing the obstruction via needle decompression (tension pneumothorax), pericardiocentesis (cardiac tamponade) or thrombolytics to dissolve a massive pulmonary embolus (PE). As you treat the underlying cause and improve the perfusion of the tissues, the levels of lactate should decrease and the pH should go up, regardless of which type of shock your patient is suffering from.
Cardiogenic: A weak or damaged heart is unable to properly circulate enough blood to perfuse the rest of the body. Its treatment focuses on trying to support the heart function and output. Powerful medications can improve the strength of the cardiac contraction; sometimes fluids can be used in moderation.
Patients in hypovolemic or distributive shock will require large volumes of fluid, but patients in cardiogenic shock will often benefit most from vasoactive medications, such as Dobutamine.
Identification of the type of shock will therefore guide your treatments. Identifying the underlying cause of the shock state is important for initiating treatment but also for identifying the most appropriate receiving hospital.
For patients with certain conditions, such as trauma or ST-elevation myocardial infarction (STEMI), bypassing the nearest hospital in favor of a more distant hospital that specializes in the condition (e.g., Level 1 trauma center or coronary catheterization lab facility) has been shown to improve outcomes for the patient.
After formulating a differential diagnosis, we can determine which of the potential life-threatening causes we can begin to reverse in the field or those for which the patient requires transfer to a specific hospital.
Table 2: Tips for Creating a Differential Diagnosis
1. Collect the necessary data via history, physical exam & ancillary data (e.g., ECG, EtCO2 reading).
2. Analyze the data to determine potential causes of the patient’s presentation (i.e., a differential diagnosis).
3. Prioritize the list of differentials with the top of the list representing the things you can correct in the field or those that would affect your hospital designation.
4. Initiate interventions to identify & correct the things on your differential diagnosis starting at the top of your list (most lethal) & ending at the bottom (most common).
5. Continually reassess to rule out or rule in the conditions listed in your differential.
For patients with chest pain, ECGs can identify STEMI, which limits the hospital designations to which we can transport these patients. Not all hospitals can accept patients in preterm labor or those with burns and major trauma.
In our case, our patient collapsed and had an elevated lactate after exertion on a hot, humid day. The initial data collection, including vital signs and, in this case, lactate measurement, found her to be in shock. Focusing your differential diagnosis on the potential causes of shock that we can most easily correct in the field is a good way to help prioritize your treatment interventions.
It’s important to remember that multiple conditions can contribute to your patient’s presentation. Consider a patient with a severe gastrointestinal (GI) bleed who shows signs of a STEMI on your ECG.
STEMI is typically treated with antiplatelet (aspirin) and anticoagulant (heparin) agents and cardiac catheterization lab activation to open a blocked artery. In a patient who’s hemorrhaging, however, anemia is the cause of their cardiac ischemia, and a coronary angiogram will reveal patent coronary arteries. This patient requires blood, not blood thinners, and administration of aspirin could have devastating consequences.
So what are the differentials for Nadifa? We re-evaluate her EtCO2 and get a reading of 21 mmHg and a respiratory rate of 24 breaths per minute. This, combined with her elevated lactate levels, suggests that she’s in acidosis. Breath sounds were hard to hear because of the noise at the fair.
Putting this data together leads to a diagnosis of shock. Our differentials would include myocardial infarction, sepsis, poisoning from the herbal supplements, severe dehydration, GI bleed, PE and anaphylaxis from an unreported bee sting during the race.
Additionally, a distant possibility that needs to remain is a spontaneous tension penumothorax during the race.
When we order this list according to our rules, we’ve gotten: anaphylaxis, spontaneous tension penumothorax, dehydration, MI, GI bleed, sepsis, poisoning. So we should prioritize our interventions by rapidly extricating the patient from the crowd into the ambulance.
With her permission, we would have inspected her skin to evaluate for rashes that would suggest anaphylaxis. Breath sounds would have been reassessed in the quiet ambulance to search for a tension penumothorax.
Large-bore IV access would have been established and volume resuscitation initiated. Her ECG showed sinus tachycardia with no ST changes or T-wave inversions. Poison control should have been contacted to see if the Haba sodah or camel’s milk could have been contributing to her shock.
Ultimately, the providers rapidly cleared the scene and initiated transport to the local community emergency department with a suspected diagnosis that was now focused on dehydration from fever, diuretics, laxatives and exertion, which was being aggressively treated with IV volume resuscitation. JEMS
Aaron Burnett, MD, is the associate medical director for Regions Hospital EMS in St. Paul Minnesota and an Assistant Professor of Emergency Medicine at the University of Minnesota. He can be reached at Aaron.M.Burnett@HealthPartners.com.
David Page, MS, NREMT-P, is an educator at Inver Hills Community College and a paramedic at Allina EMS in Minneapolis/St. Paul. He has 27 years of EMS experience and still learns something every time he responds to a call. Send him feedback at firstname.lastname@example.org.
1. Longo D, Fauci A, Kasper D, et al: Harrison’s Principles of Internal Medicine: Volumes 1 and 2, 18th Edition. McGraw-Hill Professional: New York, 2011.
2. Nickerson R. Confirmation bias: A ubiquitous phenomenon in many guises. Review of General Psychology. 1998;2(2):175–220.
3. Sato L. Evidence-based patient safety and risk management technology. J Qual Improv. 2001;27:435.
4. Plsek P. (1999). Section 1: Evidence-Based Quality Improvement Principles, and Perspectives. In Directed Creativity. Retrieved Jan. 25, 2012, from www.directedcreativity.com/pages/PlsekPeds.pdf.
5. Schiff G, Kim S, Abrams R, et al. (2004). Diagnosing Diagnosis Errors: Lessons from a Multi-institutional Collaborative Project. In Agency for Healthcare Research and Quality. Retrieved Jan. 1, 2012, from www.ahrq.gov/downloads/pub/advances/vol2/Schiff.pdf.
6. Kartal M, Eray O, Rinnert S, et al. EtCO2: A predictive tool for excluding metabolic disturbances in nonintubated patients. Am J Emerg Med. 2011;29(1):65–69.
7. Bakker J, Jansen T. Don’t take vitals, take a lactate. Intensive Care Med. 2007;33(11):1863–1865.
8. Gunnerson K. (n.d.). Lactic Acidosis. In Medscape. Retrieved Jan. 1, 2012, from http://emedicine.medscape.com/article/167027-overview.
9. Blomkalns A. (2007). Lactate: A marker for sepsis and trauma. In Emergency Medicine Cardiac Research and Education Group. Retrieved Jan. 1, 2012, from www.emcreg.org/publications/monographs/acep/2006/alb_acep2006.pdf.
10. Chapleau W, Burba A, Pons P, et al: The Paramedic, First Edition. McGraw-Hill: New York, p. 293, 2009.
11. Tintinall J, Stapczynski J, Ma O, et al: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Sixth Edition. McGraw Hill: New York, 2004.
Test your comprehension with this post-article quiz. Answers are provided at the end. Photocopying is permitted for nonprofit training purposes only. For readers in need of continuing education credits, please visit JEMSCE.com to choose from courses that are CECBEMS approved and meet NREMT refresher requirement.
1. What is a normal lactate level?
A. < 2.5 mg/dL
B. > 5 mg/dL
C. > 1 mg/dL
D. > 7.5 mg/dL
2. What type of shock is this patient displaying?
3. The patient presents with a respiratory rate of 34 and an EtCO2 reading of 21 mmHg. What should you suspect?
A. Myocardial infarction
B. Overdose of herbal supplements
4. Which compensatory mechanism for shock may be masked by metoprolol?
A. Normal pulse
D. Atrial fibrillation
5. Which of the following is the most effective in energy generation?
This article originally appeared in March 2012 JEMS as “Unveiling the Condition: Use your differential diagnosis to begin ruling out causes.”