A 39-year-old male with symptomatic hypogonadism on testosterone therapy presents to the emergency department at the request of his primary care physician after outpatient labs showed a hemoglobin of 22.0 g/dl. He denies chest pain, shortness of breath, extremity swelling, or neurologic symptoms such as changes in vision, motor function, or sensation. On evaluation, his vital signs and a detailed physical examination are normal. There are no other lab abnormalities.

The patient was discharged with outpatient primary care follow-up after collection of serum EPO and JAK2 levels – the former of which was elevated and findings were attributed to testosterone use.

Algorithm for the Evaluation of Erythrocytosis

References

1. Tefferi A, Barbui T. Polycythemia vera and essential thrombocythemia: 2019 update on diagnosis, risk-stratification, and management. American Journal of Hematology. 2019;94(1):133-143. doi:10.1002/ajh.25303
2. McMullin MF, Harrison CN, Ali S, et al. A guideline for the diagnosis and management of polycythaemia vera. British Journal of Haematology. 2019;184(2):176-191. doi:10.1111/bjh.15648
3. Tintinalli JE, Ma OJ, Yealy DM, et al., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020.

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Depressed ejection fraction, image from The POCUS Atlas

An 44 year-old male with no reported medical history (though limited access to medical care) presents with lower extremity swelling. He states that the symptoms have been gradually worsening over the past 3 months. He notes occasional fatigue while at work but denies chest pain, shortness of breath, leg pain or changes in urination.

A point-of-care ultrasound is performed showing decreased left ventricular ejection fraction. The patient was admitted for further evaluation and management of new-onset congestive heart failure.

Algorithm for the Evaluation of Lower Extremity Edema with Ultrasound

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.

• DVT
• Cirrhosis
• Soft Tissue

Nodular liver contour, ascites

Ascites

Cobblestoning

Cobblestoning

Longitudinal view of a ruptured Baker cyst

References

1. Trayes KP, Studdiford JS, Pickle S, Tully AS. Edema: diagnosis and management. Am Fam Physician. 2013;88(2):102-110.
2. Goyal A, Cusick AS, Bhutta BS. Peripheral Edema. [Updated 2022 Nov 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554452/
3. Smith, C. Clinical manifestations and evaluation of edema in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed 2/11/2023.

The post Lower Extremity Edema Ultrasound appeared first on Differential Diagnosis of.

A 65-year-old male with a past medical history of hypertension, diabetes mellitus, and atrial fibrillation presents after a mechanical fall with a posterior scalp hematoma and altered mental status. The patient’s family reports that the patient is taking apixaban with his last dose 4 hours prior to arrival. Physical examination reveals a GCS of 13, blood pressure of 175/99, and asymmetric pupils. The patient is taken to CT where head imaging reveals left sided subdural hematoma with midline shift and developing uncal herniation.

A nicardipine infusion is initiated and the head of the bed is elevated. Andexanet Alfa is not available, therefore an infusion of 4-Factor PCC is initiated. The patient is taken emergently to the operating room by neurosurgery for craniotomy and hematoma evacuation.

An Algorithm for the Reversal of Anticoagulation for Intracranial Hemorrhage ^1-4

All Agents

For all agents, discontinue anticoagulation. Patients may require blood pressure control including anti-hypertensive infusions (goal SBP <140). Avoid reversal for intracranial hemorrhage associated with cerebral venous thrombosis. Use cautiously in patients with concomitant life-threatening ischemia, thrombosis, or severe DIC.

Vitamin K Antagonists (ex. warfarin)

Initial Dose

A fixed dose of 4F-PCC 1500 to 2000 units can be given as an initial dose with repeat dosing based on INR measurement 15 minutes after completion of infusion. Follow local institution guidelines if available.

Monitoring and Repeat Dosing

• Vitamin K: if INR ≥1.4 at 12 hours ⁵
• 4F-PCC: May consider repeat PCC dosing based on INR, though with increased DIC and thrombotic risk, it is recommended to correct further with FFP if INR remains ≥1.4 ⁶

Direct Factor Xa Inhibitors (ex. rivaroxaban, apixaban)

Activated charcoal may be effective for up to six hours for apixaban ⁷ and eight hours for rivaroxaban ⁸.

*Andexanet alfa Regimens ^9,10

• Low-dose: rivaroxaban <10mg, apixaban <5mg, edoxaban <30mg or 8 or more hours since last dose
• High-dose: If greater than above thresholds, or dose/timing unknown

Pentasaccharides (ex. fondaparinux)

Use high-dose Andexanet alfa regimen ¹²

Direct Thrombin inhibitors (ex. dabigatran)

Monitoring and Repeat Dosing

If ongoing significant bleeding after treatment, consider redosing idarucizumab and/or hemodialysis.

Alternative Regimens

If idarucizumab is not available, aPCC (50-80 units/kg) , 4F-PCC or 3F-PCC (50 units/kg) can be used in order of preference.

Unfractionated Heparin

Dosing

Determination of units of heparin is based on estimated active agent (half-life 1-2 hours)

• Protamine sulfate 1mg/100 units IV, maximum dose 50mg
• Alternatively, can give fixed dose of 25-50mg

Monitoring and Repeat Dosing

If aPTT is persistently elevated, repeat 0.5 mg/100 units

Low-Molecular Weight Heparin ¹³

Reversal is not indicated if more than 3-5 half-lives have passed since administration:

• Enoxaparin mean half-life: 4-5 hours
• Dalteparin mean half-life: 2.8 hours
• Nadroparin mean half-life: 3.7 hours

If bleeding persists, or renal insufficiency, repeat dose .5 mg/1 mg enoxaparin or .5 mg/100 anti-Xa units.

References

Guidelines & Reviews

1. Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 guideline for the management of patients with spontaneous intracerebral hemorrhage: a guideline from the american heart association/american stroke association. Stroke. Published online May 17, 2022:101161STR0000000000000407.
2. Tomaselli GF, Mahaffey KW, Cuker A, et al. 2020 acc expert consensus decision pathway on management of bleeding in patients on oral anticoagulants: a report of the american college of cardiology solution set oversight committee. J Am Coll Cardiol. 2020;76(5):594-622.
3. Frontera JA, Lewin JJ, Rabinstein AA, et al. Guideline for reversal of antithrombotics in intracranial hemorrhage: a statement for healthcare professionals from the neurocritical care society and society of critical care medicine. Neurocrit Care. 2016;24(1):6-46.
4.  Freeman, W. David, Weitz, Jeffrey. “Reversal of anticoagulation in intracranial hemorrhage.” UpToDate. (2022) https://www.uptodate.com/contents/reversal-of-anticoagulation-in-intracranial-hemorrhage?search=anticoagulation%20reversal (Accessed on May 26, 2022)

Vitamin K Antagonists

5. Ansell J, Hirsh J, Hylek E, Jacobson A, Crowther M, Palareti G. Pharmacology and management of the vitamin k antagonists: american college of chest physicians evidence-based clinical practice guidelines(8th edition). Chest. 2008;133(6 Suppl):160S-198S.
6. Pabinger I, Brenner B, Kalina U, et al. Prothrombin complex concentrate (Beriplex p/n) for emergency anticoagulation reversal: a prospective multinational clinical trial. J Thromb Haemost. 2008;6(4):622-631.

Direct Factor Xa Inhibitors

7. http://packageinserts.bms.com/pi/pi_eliquis.pdf
8. https://www.bayer.com/sites/default/files/2020-11/xarelto-pm-en.pdf
9. Demchuk AM, Yue P, Zotova E, et al. Hemostatic efficacy and anti-fxa (Factor xa) reversal with andexanet alfa in intracranial hemorrhage: annexa-4 substudy. Stroke. 2021;52(6):2096-2105.
10. Cohen AT, Lewis M, Connor A, et al. Thirty-day mortality with andexanet alfa compared with prothrombin complex concentrate therapy for life-threatening direct oral anticoagulant-related bleeding. J Am Coll Emerg Physicians Open. 2022;3(2):e12655.
11. Scaglione F. New oral anticoagulants: comparative pharmacology with vitamin K antagonists. Clin Pharmacokinet. 2013;52(2):69-82.

Pentasaccharides (ex. fondaparinux)

12. Lu G, DeGuzman FR, Hollenbach SJ, et al. A specific antidote for reversal of anticoagulation by direct and indirect inhibitors of coagulation factor Xa. Nat Med. 2013;19(4):446-451.

Low-Molecular Weight Heparin

13. Fareed J, Hoppensteadt D, Walenga J, et al. Pharmacodynamic and pharmacokinetic properties of enoxaparin : implications for clinical practice. Clin Pharmacokinet. 2003;42(12):1043-1057.

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A 66 year-old male with a history of hypertension and COPD presents with shortness of breath. He states that his symptoms are unimproved with home nebulizer treatments and denies fever, cough or new sputum production. On examination, he has stridor appreciated during inspiratory and expiratory phases.

Sound Characteristics

Respiratory Phase

Inspiratory

Supraglottic: negative intratracheal pressure during inspiration causes airway collapse.

Biphasic

Glottic/Subglottic: fixed obstruction not impacted by changes in luminal/thoracic pressure.

Expiratory

Intrathoracic: increased pleural pressure compresses the narrowed airway.

An Algorithm for the Diagnosis of Wheezing and Stridor

References

1. Sicari V, Zabbo CP. Stridor. [Updated 2021 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK525995/
2. Patel PH, Mirabile VS, Sharma S. Wheezing. [Updated 2021 May 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482454/
3. Bohadana A, Izbicki G, Kraman SS. Fundamentals of lung auscultation. N Engl J Med. 2014;370(21):2053.
4. Orient JM, Sapira JD. Sapira’s Art & Science of Bedside Diagnosis. 4th ed. Wolters Kluwer Health/Lippincott Williams & Wilkins; 2010.

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A 48 year-old male with a history of congestive heart failure s/p left ventricular assist device is brought in by EMS with low-flow alarms. According to prehospital report, the patient had otherwise been in his usual state of health and had been shocked by his ICD multiple times prior to their arrival. No vital signs could be obtained en route.

On arrival in the emergency department, the patient was awake and responding appropriately to questions. His MAP was 80mmHg, an audible whir was auscultated from his device and the skin surrounding the percutaneous exit site appeared normal.

ECG

POCUS

The patient’s device was inactivated with a magnet to prevent further ineffectual shocks. An arterial line was placed for continuous blood pressure measurement. He was sedated and externally defibrillated with return to normal sinus rhythm prior to admission to the CCU.

An Algorithm for the Evaluation of Unstable LVAD¹

Reference

Stenberg R, Shenvi C. Targeted evaluation of patients with left ventricular assist devices and shock or hypotension. Ann Emerg Med. 2020;76(1):34-41.

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A 40 year-old male with a history of diabetes presents after accidental insulin overdose. He reports inadvertently administering 50 units of rapid-acting insulin when intending to take his long-acting insulin 25 minutes prior to presentation. He is currently asymptomatic, has a normal physical examination and his point-of-care glucose is 65mg/dL.

ED Course

The patient’s insulin regimen was clarified:

• Insulin glargine 50 units SQ once daily
• Insulin aspart 1 unit per 5g carbohydrates SQ before meals

The patient administered an insulin dose sufficient to dispose of 250g of carbohydrates with an impending peak action within minutes. The required dose of parenteral dextrose would require potentially-toxic^1,2 solution concentrations (one liter of D25 or 10 ampules of D50) and there was insufficient time for central venous catheter placement. Moreover, the patient was awake and asymptomatic – able to tolerate oral intake. Juice boxes containing 15g of carbohydrates each were located and the patient drank 16-17 boxes while undergoing serial glucose measurements. His blood glucose ranged between 70mg/dL and 150mg/dL and he was discharged after an uneventful 6-hour observation.

Insulin Pharmacokinetics³

Insulin and Carbohydrates

The effects of both insulin and carbohydrate ingestion on blood glucose are individualized. If known, the patient’s insulin:carbohydrate ratio can be used to anticipate the effect of overdose. Alternatively, their mealtime dose and carbohydrate allowance can be used.

Very broadly, one gram of carbohydrates increases blood glucose by 3-5mg/dL and one unit of insulin disposes of 10 grams of carbohydrates (or reduces blood glucose by 30-50mg/dL).⁴

Differential Diagnosis of Hypoglycemia

Common Anti-hyperglycemic Drugs and Pharmacology

Evaluation of Hypoglycemia

Patients with known diabetes who are not systemically ill and can identify a clear precipitant, no extensive workup is required. In severely ill patients, consider:

• BMP
• LFT
• EtOH
• Infectious workup: CXR, UA, urine and blood cultures
• ECG, troponin
• Other studies: insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies

Management and Monitoring

References:

1. Kuwahara T, Asanami S, Kubo S. Experimental infusion phlebitis: tolerance osmolality of peripheral venous endothelial cells. Nutrition. 1998;14(6):496-501.
2. Wiegand R, Brown J. Hyaluronidase for the management of dextrose extravasation. Am J Emerg Med. 2010;28(2):257.e1-2.
3. Hirsch IB. Insulin analogues. N Engl J Med. 2005;352(2):174-183.
4. Your Insulin Therapy. (2004). Am Fam Physician, 70(3), 511-512.
5. Self, W. H., & McNaughton, C. D. (2013). Hypoglycemia. In Emergency Medicine (2nd ed., pp. 1379-1390). Elsevier.
6. Service, FJ. Hypoglycemia in adults: Clinical manifestations, definition, and causes. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on March 18, 2016.)
7. Service FJ. Hypoglycemic disorders. N Engl J Med. 1995;332(17):1144–1152. doi:10.1056/NEJM199504273321707.
8. Krinsley JS, Grover A. Severe hypoglycemia in critically ill patients: risk factors and outcomes. Critical Care Medicine. 2007;35(10):2262–2267. doi:10.1097/01.CCM.0000282073.98414.4B.
9. Lacherade J-C, Jacqueminet S, Preiser J-C. An overview of hypoglycemia in the critically ill. J Diabetes Sci Technol. 2009;3(6):1242–1249.

The post Hypoglycemia appeared first on Differential Diagnosis of.

A 38 year-old male with unknown medical history is brought to the emergency department by EMS with agitation and bizarre behavior. According to prehospital report, the patient was acting erratically – shouting incomprehensibly in the middle of a busy street with possible associated seizure activity.

On evaluation, the patient was found to be tachycardic, hypertensive, and markedly agitated. Physical examination with a focus on toxidromes was notable for the presence of rotary nystagmus suggestive of hallucinogen including phencyclidine toxicity. The patient required pharmacologic sedation to allow for a broad evaluation of altered mental status.

ED Course

The patient’s workup including core temperature, head imaging and laboratory tests (including AST/ALT, albumin, INR) were unremarkable with the exception of an ammonia level of 142 umol/L (normal range 16-53), slightly elevated CK, and urine toxicology screen with multiple positive agents. Over the course of several hours in the emergency department, the patient’s mental status gradually improved reaching normal level of alertness and orientation with normal neurological examination. He acknowledged PCP use as well as a prior history of seizures (possibly related to ethanol withdrawal) without routine anti-epileptic drug use. He denied known history of liver disease.

The patient’s hyperammonemia was attributed to a hypercatabolic state secondary to phencyclidine-induced agitation with possible seizure. He was discharged with resources for assistance with substance cessation.

An Algorithm for the Differential Diagnosis of Hyperammonemia:

References:

1. Kalra A, Norvell JP. Cause for Confusion: Noncirrhotic Hyperammonemic Encephalopathy. Clin Liver Dis. 2020;15(6):223-227. doi:10.1002/cld.929
2. Mallet M, Weiss N, Thabut D, Rudler M. Why and when to measure ammonemia in cirrhosis? Clin Res Hepatol Gas. 2018;42(6):505-511. doi:10.1016/j.clinre.2018.01.004
3. Hassan AAI, Ibrahim W, Subahi A, Mohamed A. ‘All that glitters is not gold’: when hyperammonaemia is not from hepatic aetiology. Bmj Case Reports. 2017;2017:bcr-2017-219441. doi:10.1136/bcr-2017-219441
4. Odigwe CC, Khatiwada B, Holbrook C, et al. Noncirrhotic Hyperammonemia Causing Relapsing Altered Mental Status. Bayl Univ Medical Cent Proc. 2017;28(4):472-474. doi:10.1080/08998280.2015.11929312
5. Upadhyay R, Bleck TP, Busl KM. Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature. Case Reports Medicine. 2016;2016:1-10. doi:10.1155/2016/8512721
6. Walker V. Severe hyperammonaemia in adults not explained by liver disease. Ann Clin Biochem. 2011;49(3):214-228. doi:10.1258/acb.2011.011206
7. Laish I, Ari ZB. Noncirrhotic hyperammonaemic encephalopathy. Liver Int. 2011;31(9):1259-1270. doi:10.1111/j.1478-3231.2011.02550.x
8. LaBuzetta JN, Yao JZ, Bourque DL, Zivin J. Adult Nonhepatic Hyperammonemia: A Case Report and Differential Diagnosis. Am J Medicine. 2010;123(10):885-891. doi:10.1016/j.amjmed.2010.02.029
9. Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest. 2007;132(4):1368-1378. doi:10.1378/chest.06-2940
10. Weng T-I, Shih FF-Y, Chen W-J. Unusual causes of hyperammonemia in the ED. Am J Emerg Medicine. 2004;22(2):105-107. doi:10.1016/j.ajem.2003.12.011
11. Hawkes ND, Thomas GAO, Jurewicz A, et al. Non-hepatic hyperammonaemia: an important, potentially reversible cause of encephalopathy. Postgrad Med J. 2001;77(913):717. doi:10.1136/pmj.77.913.717

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A 65 year-old female with a history of hypertension, hyperlipidemia and rheumatoid arthritis presents with generalized weakness and nausea/vomiting for 3 days. She denies fever, focal weakness, numbness or speech difficulty.

HPA Axis

Vital signs were notable for hypotension (72/48mmHg), her examination revealed diffuse weakness but no focal deficits and her abdominal examination was unremarkable. Laboratory tests were notable for hyponatremia (117 mEq/L) and new renal dysfunction. She received 2L of intravenous fluids but remained hypotensive.

Additional history revealed that the patient had been out of her home medications (including prednisone) for the past 1 week. Samples for laboratory tests (cortisol, ACTH) were drawn and she was treated with hydrocortisone 100mg IV with subsequent improvement in blood pressure – she was admitted to the ICU for adrenal crisis.

An Algorithm for the Evaluation and Management of Adrenal Insufficiency and Crisis

References:

1. Idrose, A., Tintinalli, J., Ma, O., Yealy, D., Meckler, G., Stapczynski, J., Cline, D., Thomas, S. (2020). Adrenal Insufficiency Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e
2. Carroll, T., Aron, D., Findling, J., Tyrrell, J., Gardner, D., Shoback, D. (2017). Glucocorticoids and Adrenal Androgens Greenspan’s Basic & Clinical Endocrinology, 10e
3. Dineen, R., Thompson, C., Sherlock, M. (2019). Adrenal crisis: prevention and management in adult patients Therapeutic Advances in Endocrinology and Metabolism 10(), 2042018819848218. https://dx.doi.org/10.1177/2042018819848218
4. Rushworth, R., Torpy, D., Falhammar, H. (2019). Adrenal Crisis New England Journal of Medicine 381(9), 852-861. https://dx.doi.org/10.1056/nejmra1807486
5. Amrein, K., Martucci, G., Hahner, S. (2018). Understanding adrenal crisis Intensive Care Medicine 44(5), 652-655. https://dx.doi.org/10.1007/s00134-017-4954-2
6. Oelkers, W. (1996). Adrenal Insufficiency The New England Journal of Medicine 335(16), 1206-1212. https://dx.doi.org/10.1056/nejm199610173351607
7. Tucci, V., Sokari, T. (2014). The Clinical Manifestations, Diagnosis, and Treatment of Adrenal Emergencies Emergency Medicine Clinics of North America 32(2), 465-484. https://dx.doi.org/10.1016/j.emc.2014.01.006
8. Bleicken, B., Hahner, S., Ventz, M., Quinkler, M. (2010). Delayed Diagnosis of Adrenal Insufficiency Is Common: A Cross-Sectional Study in 216 Patients The American Journal of the Medical Sciences 339(6), 525-531. https://dx.doi.org/10.1097/maj.0b013e3181db6b7a
9. Broersen, L., Pereira, A., Jørgensen, J., Dekkers, O. (2015). Adrenal Insufficiency in Corticosteroids Use: Systematic Review and Meta-Analysis The Journal of Clinical Endocrinology & Metabolism 100(6), 2171-2180. https://dx.doi.org/10.1210/jc.2015-1218
10. Joseph, R., Hunter, A., Ray, D., Dixon, W. (2016). Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review Seminars in Arthritis and Rheumatism 46(1), 133-141. https://dx.doi.org/10.1016/j.semarthrit.2016.03.001

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References

1. Siegel, J., Rhinehart, E., Jackson, M., Chiarello, L., Committee, H. (2007). 2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Health Care Settings American Journal of Infection Control 35(10), S65-S164. https://dx.doi.org/10.1016/j.ajic.2007.10.007
2. Liang, S., Theodoro, D., Schuur, J., Marschall, J. (2014). Infection Prevention in the Emergency Department Annals of Emergency Medicine 64(3), 299-313. https://dx.doi.org/10.1016/j.annemergmed.2014.02.024
3. Liang, S., Riethman, M., Fox, J. (2018). Infection Prevention for the Emergency Department: Out of Reach or Standard of Care? Emergency medicine clinics of North America 36(4), 873-887. https://dx.doi.org/10.1016/j.emc.2018.06.013
4. Gottenborg, E., Barron, M. (2016). Isolation Precautions in the Inpatient Setting Hospital Medicine Clinics 5(1), 30-42. https://dx.doi.org/10.1016/j.ehmc.2015.08.004
5. Harding, A., Almquist, L., Hashemi, S. (2011). The use and need for standard precautions and transmission-based precautions in the emergency department. Journal of emergency nursing: JEN : official publication of the Emergency Department Nurses Association 37(4), 367-73; quiz 424-5. https://dx.doi.org/10.1016/j.jen.2010.11.017

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A 67 year-old male with a history of hypertension and diabetes presents to the emergency department after a syncopal episode. He had been completing his normal morning routine when he developed a sensation of lightheadedness and awoke on the ground of his kitchen. He denies associated chest pain, palpitations, diaphoresis, or recent illness. He has no known sick contacts nor exposures to individuals undergoing evaluation for COVID-19.

On arrival in the emergency department, the patient was noted to be hypoxic with pulse oximetry measuring 74%. He was placed on supplemental oxygen via non-rebreather with improvement of oxygen saturation to 94%. Examination demonstrated diminished alertness (requiring constant stimulation for responses) and generalized motor weakness. Cardiac and pulmonary examinations were unremarkable with the exception of tachypnea and no extremity edema was appreciated.

A chest radiograph was obtained which demonstrated platelike atelectasis. An arterial blood gas was obtained with PaO₂ of 72mmHg suggesting a prominent A-a gradient. CT pulmonary angiography was obtained:

Upon return, the patient’s mental status worsened associated with hypotension and he was intubated for airway protection and received systemic thrombolysis. He was subsequently taken for emergent endovascular treatment of massive pulmonary embolus.

An Algorithm for the Differential Diagnosis of Hypoxemia & Hypoxia^1-7

Hypoxemia is defined as low PaO₂ while hypoxia is insufficient global or local tissue oxygen content.

References

1. Stapczynski J. Respiratory Distress. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219642010. Accessed April 12, 2020.
2. Gas Transport & pH. In: Barrett KE, Barman SM, Brooks HL, Yuan JJ. eds. Ganong’s Review of Medical Physiology, 26e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2525&sectionid=204297654. Accessed April 12, 2020.
3. Loscalzo J. Hypoxia and Cyanosis. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2129&sectionid=192012521. Accessed April 12, 2020.
4. West NE, Lechtzin N. Chapter 93. Hypoxia. In: McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS. eds. Principles and Practice of Hospital Medicine New York, NY: McGraw-Hill; 2012. http://accessmedicine.mhmedical.com/content.aspx?bookid=496&sectionid=41304065. Accessed April 12, 2020.
5. Pulmonary Physiology. In: Kibble JD, Halsey CR. eds. Medical Physiology: The Big Picture New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/content.aspx?bookid=1291&sectionid=75576764. Accessed April 12, 2020.
6. Petersson, J., Glenny, R. (2014). Gas exchange and ventilation–perfusion relationships in the lung European Respiratory Journal 44(4), 1023-1041. https://dx.doi.org/10.1183/09031936.00037014
7. Morchi, R. (2011). Diagnosis Deconstructed: The Case of the Patient with No Chief Complaint Emergency Medicine News XXXIII(3)
   Rodríguez-Roisin, R., Roca, J. (2005). Mechanisms of hypoxemia Intensive Care Medicine 31(8), 1017-1019. https://dx.doi.org/10.1007/s00134-005-2678-1

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