Hyperkalemia (2024)

by Chelsea N. Allen

You have a new patient!

A 58-year-old female is brought into the emergency department (ED) by her family for dizziness and fatigue that started today. She has a history of hypertension for which she takes a calcium channel blocker and end-stage renal disease (ESRD) and has been on dialysis for the last four years. She did miss her dialysis session today due to her symptoms, with her last session four days ago.

At triage, her vital signs are as follows: BP 170/90 mmHg, HR 30/min, RR of 18/min, temperature 37.1 degrees Celsius, SpO2 of 98% on room air. She appears fatigued but is able to answer questions appropriately and has no obvious focal neurologic deficits.

Triage EKG is below

What do you need to know?

Hyperkalemia is one of the most important electrolyte abnormalities you will encounter in the emergency department (ED), given the potential for cardiac arrest in these patients. It refers to when the serum potassium (K) is greater than 5.5mEq/L. In all patients suspected of hyperkalemia, it is essential to place them on a cardiac monitor, obtain IV access, and perform an EKG due to the significant role potassium plays in the cardiac cycle. These patients may have non-specific symptoms, such as weakness and fatigue, and thus can make it hard to discern the diagnosis up front. Patients with a high pretest probability, such as those who miss dialysis or have had prior episodes of hyperkalemia, are usually treated for hyperkalemia before lab results are available due to the potential life-threatening nature of the condition. Potassium is stored in the body’s cells. It can be excreted during cellular damage, such as in rhabdomyolysis, or during certain physiologic states to balance the body’s pH when the serum becomes acidotic (e.g., DKA) [1,2].  Potassium is then excreted from the body by the kidneys/urinary system, so in patients whose kidney function has declined, such as ESRD, or in patients with an obstruction (bladder stone, enlarged prostate), potassium must be excreted through dialysis or by removal.

Medical History

Patients with hyperkalemia often present with non-specific symptoms, such as fatigue, muscle weakness, and cramps, which can often lead to a delay in the diagnosis and can be detrimental, even fatal to the patient. Elevations of potassium in a patient’s serum can be caused when there is a disruption in the storage or excretion mechanisms in the body and can cause cardiac arrhythmias, such as premature beats (PVCs), irregular beats (atrial fibrillation) or cardiac arrest (ventricular fibrillation) due to the role of potassium in regulating the cardiac membrane potential [1-5]. Since an underlying elevation in potassium can cause these non-specific symptoms, it is imperative to do a thorough history, keying in on a history of kidney issues, dialysis appointments, and urinary symptoms.

Physical Examination

The most crucial physical exam components in patients with hyperkalemia are the cardiac and skin exam, especially in patients who may not be able to give you much information, as a thorough skin exam can elicit an AV fistula/graft or tunnel catheter, which would clue you into the patient being on dialysis. If the patient does not have a history of ESRD on dialysis, the cardiac exam could be another clue, elucidating irregular rhythms or bradycardia and prompting you to get further evaluation with an EKG.

Alternative & Differential Diagnoses

Given that hyperkalemia can cause a myriad of non-specific symptoms, patients can sometimes have a long list of differential diagnoses. Outside of the cardiac complications, hyperkalemia can cause muscle cramping, fatigue, or feeling weak. Unless you have a high index of suspicion, these symptoms can be attributed to muscle strains or viral illnesses, which in patients who are otherwise healthy or have a good history of these may be more likely than hyperkalemia [5].

Acing Diagnostic Testing

One of the most important tests for patients suspected of having hyperkalemia is the EKG, given how quickly this bedside test can be performed and the wealth of information that can be obtained, especially regarding electrolytes [4,5]. The classic EKG finding in patients with hyperkalemia is peaked T waves. However, hyperkalemia can mimic many EKG changes, and other findings suggest hyperkalemia are a widened QRS, flattened P waves, and heart blocks [3,4,5]. The EKG may follow a step-wise pattern of peaked T waves, followed by progressively lengthening QRS. However, generally, they do not always follow this pattern, so it is important to have a high index of suspicion when you see these changes. The next step is usually laboratory testing with a basic metabolic panel to confirm hyperkalemia. It can also indicate the patient’s electrolyte levels, provide insight into their acid-base balance, and suggest other potential diagnoses. You may also get other testing depending on the cause of the hyperkalemia, such as CT or US imaging, if urinary tract obstruction is the suspected cause. However, in general, imaging is not needed to make the diagnosis.

Risk Stratification

Most of the patients with hyperkalemia are going to be chronic kidney disease or dialysis patients, which are inherently at higher risk given their underlying disease process as well as the fact that the kidneys process and excrete potassium in the body. Specifically, anuric patients within this group are going to be at higher risk for complications, given that the only way to excrete potassium is through dialysis, putting them at risk for the potentially fatal complications of hyperkalemia [1,2].

Management

As always, following the ABCs of emergent patient management is crucial in deciding how quickly you need to intervene, especially in hyperkalemic patients, where cardiac arrest is a high possibility. Once you have assessed that your patient has a patent airway by speaking to them, their breathing by listening for bilateral breath sounds, and their circulation by ensuring they have a pulse, the next critical step in managing hyperkalemia is the reduction of potassium within the body and serum. This is achieved in two ways: shifting and elimination [2,3,4,5]. One medication we use in hyperkalemia where we have EKG changes attributed to elevations in potassium is Calcium (gluconate or chloride) which the sole purpose of this medication is stabilization of the cardiac membrane to prevent further deterioration into unstable rhythms and is usually given first in the line of medications [2]. Its onset is rapid (15-30 min) with a duration of 30-60 min. Monitor closely as it does not lower potassium but rather protects the heart. Calcium chloride is more concentrated than calcium gluconate, so it requires a central line due to the risk of tissue damage.

Shifting medications will be Insulin and Albuterol, given that these medications work in the cAMP pathway on the cell membranes, causing extracellular potassium to shift intracellularly, thereby transiently decreasing serum potassium. Dextrose is usually given with insulin to prevent the drop in glucose associated with insulin use, and it does not shift/eliminate potassium, but it is still vital. If your patient is able to make urine, giving a dose of Furosemide (or another potassium-depleting diuretic) is useful to help start the process of potassium elimination, as these medications will pull extracellular potassium into the waste product (urine). If your patient is unable to make urine, giving Sodium zirconium cyclosilicate, a potassium binder in your gastrointestinal tract, to help eliminate potassium is another way to help deplete body potassium. If severe enough (e.g., arrhythmias/cardiac arrests, ESRD patients), most patients will need to undergo hemodialysis for definitive treatment/removal of potassium. Listed below are the medications mentioned above, as well as the recommended doses and frequency.

Table: Medications frequently used in hyperkalemia treatment [5,6]

Drug generic Name

Dose

Effect

Duration

Pregnancy

Cautions / Comments

Calcium gluconate

1-3gm IV

15-30min

30-60min

C, only if clearly needed

 

Calcium chloride

1gm IV

15-30min

30-60min

C, only if clearly needed

Concentrated Calcium, needs central line

Albuterol

15-20mg nebulized

30min

2hrs

C

 

Insulin/Dextrose

10u Regular insulin IV; 25-50gm of 50% dextrose IV

30min-45min

3-6hrs

B (insulin); C (dextrose)

Usually given together, but can be omitted if Glucose >300

Furosemide

40-80mg IV

15-20min

2hrs

C

 

Sodium zirconium cyclosilicate

10mg TID PO

Can take up to 48hrs

 

Not Assigned

Usually not first line in the ED

Special Patient Groups

Given its life-threatening nature, hyperkalemia is generally treated the same way in all patient populations, including children and pregnant patients [5]. The above medications are all for adults, but they do have weight-based dosing for pediatric patients that is easily accessible on Broselow tapes found in the Emergency Department. Additional considerations for each group as follows;

Pediatrics

Hyperkalemia in children is often linked to kidney insufficiency, acidosis, and certain genetic conditions affecting potassium balance [7]. Pediatric hyperkalemia treatment includes insulin-glucose therapy, calcium gluconate, and sometimes sodium bicarbonate for acidosis [7]. Dosing is weight-based; careful monitoring is essential to prevent hypoglycemia following insulin administration [7].

Geriatrics

Older adults are prone to hyperkalemia due to decreased renal function and polypharmacy, especially with medications like ACE inhibitors and potassium-sparing diuretics [8]. Geriatric patients require slower dose titration and close monitoring of cardiac function. Reducing or discontinuing potassium-elevating medications may be prioritized before more invasive treatments. Assessing patient’s medication profile carefully to minimize potential interactions and electrolyte disturbances is important.

Pregnant Patients

Hyperkalemia is rare in pregnancy but may occur due to conditions like preeclampsia or excessive potassium supplementation. Treatment is similar to that of the general population but focuses on the safety of both the mother and fetus. Agents like insulin-glucose therapy are used with caution, and glucose and potassium levels are monitored closely to avoid fetal complications.

Caution!

The drugs listed in the table do have specific considerations for pediatric, geriatric, and pregnant patients, as follows:

  1. Calcium Gluconate and Calcium Chloride:
    • Pregnant Patients: Generally considered safe for use when needed (Pregnancy Category C), but only administered if benefits outweigh the risks due to limited data on safety in pregnancy.
    • Pediatrics: Dosing is usually adjusted based on weight, and administration must be done with caution due to the risk of tissue necrosis with calcium chloride if extravasation occurs.
  2. Albuterol:
    • Pregnant Patients: Classified as Category C. Used in asthma or bronchospasm, but risks must be considered, as inhaled bronchodilators are typically preferred.
    • Pediatrics and Geriatrics: Pediatric dosing is weight-based, while elderly patients may require lower doses due to sensitivity to stimulants.
  3. Insulin/Dextrose:
    • Pregnancy: Insulin is preferred for managing blood glucose in pregnant women with diabetes, categorized as B for insulin, while dextrose is safe when needed.
    • Pediatrics: Used in hyperkalemia or diabetic ketoacidosis with dose adjustments based on age and weight.
  4. Furosemide:
    • Geriatrics: Lower doses are generally recommended due to increased risk of dehydration and electrolyte imbalance.
    • Pregnancy: Considered Category C, used only if necessary as it may affect fetal renal development.
  5. Sodium Zirconium Cyclosilicate:
    • Limited data on its use in pediatric and pregnant populations, and generally not a first-line treatment in the emergency department for these groups.

Infographic

Hyperkalemia

When To Admit This Patient

There are very few instances where hyperkalemic patients will be discharged from the ED, given the potential life-threatening arrhythmias. However, ESRD patients who receive dialysis, are back to their baseline and have to follow up/able to make it to their scheduled dialysis sessions will most likely be able to be discharged if a cause for their hyperkalemia is something simple, such as missed dialysis appointments. Ensure clear, specific follow-up arrangements to minimize recurrence risk. Confirm with her dialysis provider for her next sessions. Most other patients will be admitted for monitoring to ensure their potassium levels are normalizing and to identify a cause.

Revisiting Your Patient

As you recall, we had a 58-year-old female with dizziness/fatigue who had missed her dialysis session and was found to be bradycardic and hyperkalemic on her initial workup. She was initially treated with calcium gluconate with improvement in her EKG as well as her symptoms and was able to receive dialysis in the ED. After a brief period of observation after her dialysis sessions and repeat BMP showing normalization of her potassium, she was discharged home with her family to continue her outpatient dialysis schedule.

Author

Picture of Chelsea N. Allen, DO

Chelsea N. Allen, DO

Originally from Adel, GA, USA, graduated college with a degree in biology from Columbus State University in Columbus, GA, USA. Then attended medical school at the Edward Via College of Osteopathic Medicine in Auburn, AL before completing her emergency Medicine residency at the University of Florida, Jacksonville, in Jacksonville, FL, USA. She is currently the Assistant Program Director for the Emergency Medicine program at UF-Jacksonville as well.

Listen to the chapter

References

  1. Harris AN, Grimm PR, Lee HW, et al. Mechanism of Hyperkalemia-Induced Metabolic Acidosis. Journal of the American Society of Nephrology. 2018;29(5):1411-1425. doi:https://doi.org/10.1681/ASN.2017111163
  2. Mount D. Potassium balance in acid-base disorders. Accessed: November 14, 2024. https://www.uptodate.com/contents/potassium-balance-in-acid-base-disorders.
  3. Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med. 2020;27(5):329-337. doi:10.1097/MEJ.0000000000000691
  4. Helman, A, Baimel, M, Etchells, E. Emergency Management of Hyperkalemia. Emergency Medicine Cases. September, 2016. Accessed November 14, 2024. https://emergencymedicinecases.com/alcohol-withdrawal-delirium-tremens/
  5. Wachira BW. Fluids, Electrolytes, and Acid-Base Disorders. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e. McGraw-Hill Education; 2017. Accessed November 14, 2024. https://accessemergencymedicine-mhmedical-com.uaeu.idm.oclc.org/content.aspx?bookid=2158&sectionid=162269029
  6. Rafique Z, Peacock F, Armstead T, et al. Hyperkalemia management in the emergency department: An expert panel consensus. J Am Coll Emerg Physicians Open. 2021;2(5):e12572. Published 2021 Oct 1. doi:10.1002/emp2.12572
  7. Lederer Hyperkalemia. Accessed: November 14, 2024. https://emedicine.medscape.com/article/240903-overview?form=fpf
  8. Ortiz A, Galán CDA, Carlos Fernández-García J, et al. Consensus document on the management of hyperkalemia. Nefrologia (Engl Ed). 2023;43(6):765-782. doi:10.1016/j.nefroe.2023.12.002

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

From Missed Hemodialysis to Multiple Arrhythmias

From Missed Hemodialysis to Multiple Arrhythmias

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.

Vitals

HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)

ECG

ECG on presentation
Monomorphic ventricular tachycardia

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern. 

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters. 

after hemodialysis

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

  1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
  2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
  3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
  4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
  5. What was the necessity for carrying out SLED for this patient?
  6. Why was this patient not immediately cardioverted in the ER?
  7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
  8. How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

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Question Of The Day #3

question of the day
question of the day 3

Which of the following is the most appropriate next step in management for this patient‘s condition?

Choice A (IV 1,000mL of 0.9% NaCl) is an isotonic crystalloid fluid helpful in a patient with depleted intravascular volume (i.e., dehydration). This patient is clinically dehydrated (dry oral mucosa and mild tachycardia); however, hypertonic 3% NaCl is a more appropriate initial treatment. Choice B (IV 50mL of 25g dextrose solution, or commonly known as “D50”) is an appropriate treatment for a patient with hypoglycemia. Checking a glucose level is a crucial part of the initial assessment of all patients with altered mental status, but this patient has a reported normal glucose level. Choice D (IV 40mg Furosemide) is a diuretic that would worsen this patient’s dehydration and acute kidney injury. This patient has severe hyponatremia along with neurological symptoms (coma and seizure). Hyponatremia plus neurologic symptoms, like vomiting, seizures, reduced consciousness, cardiorespiratory arrest, necessitate rapid correction of sodium with hypertonic (3%) NaCl solution. 3% NaCl solution can be infused 100-150mL over 15-20min and repeated up to 3 doses total. A serum sodium level should be measured after each administration of 3% NaCl in order to limit the increase in the sodium level to no more than 8-12 mEq/L over the first 24hours. This is done to reduce the risk of osmotic demyelination syndrome. Correct Answer: C

Reference

Petrino R, Marino R. Fluids and Electrolytes. “Chapter 17: Fluids and Electrolytes”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

[cite]

Hyperkalemia Treatment – Infographic

hyperkalemia treatment
Hyperkalemia

Further Reading

Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec;36(12):3246-51. doi: 10.1097/CCM.0b013e31818f22b. Review. PubMed PMID: 18936701.

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Clinical Video: abnormal hand twitching

Case Presentation

A 43-year-old female presented with altered mental status (GCS of 10/15) and abnormal twitching of hand. Reported to have a long-standing history of constipation and had been on laxatives. POC electrolytes showed Sodium: 110 mmol/L, Potassium: 3.5 mmol/L and Calcium: 0.71 mmol/L. The case managed as symptomatic euvolemic hyponatremia, hypocalcemia, and SIADHS.

Symptoms of hypocalcemia

Numbness and/or tingling of the hands, feet, or lips, muscle cramps, muscle spasms, seizures, facial twitching, muscle weakness, lightheadedness, and bradycardia.

Symptoms of hyponatremia

Nausea and vomiting, headache, confusion, loss of energy, drowsiness and fatigue, restlessness and irritability. muscle weakness, spasms or cramps, seizures, coma.

At the presentation time of the patient, you may not know these muscle spasms are because of hypocalcemia and hyponatremia’s similar symptoms. So, laboratory tests can clarify the diagnosis. However, in this case, both (Ca and Na) are low. So, you treat both. 

In addition

There are two findings related to hypocalcemia which worth to mention. Chvostek’s sign is the twitching of the facial muscles in response to tapping over the area of the facial nerve. Trousseau’s sign is carpopedal spasm caused by inflating the blood pressure cuff to a level above systolic pressure for 3 minutes. This video shows both findings.

Do you need more free clinical images or videos for your exams or presentations? Please visit iEM clinical image and video archive in Flickr and YouTube!

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Hypoglycemia by Rok Petrovčič from Slovenia

Hypoglycemia chapter written by Rok Petrovcic from Slovenia is just uploaded to the Website!

Sugar

A 75-year-old woman was brought to the emergency department by her relatives for “not being her usual self” for a day. She was on insulin therapy for her diabetes, but otherwise healthy.

On examination, she appeared confused and disoriented. Her vitals were as follow her rate 95/min, respiratory rate 18/min, blood pressure 141 over 85mmHg, T 37.7°C and SP O2 99% on room air. Given her past medical history, capillary blood glucose test was performed by the bedside. It was 2.6 mmol/L equal to 47 mg/dL, and hypoglycemia was diagnosed.

She was given a bolus dose of intravenous glucose and much to the relatives’ relief and amazement; she returned to her normal behavior within 5 minutes. The patient herself reported lower urinary tract symptoms with a low-grade fever for the last two days. In addition, blood investigation showed that her renal function had also deteriorated significantly since her last primary care visit while continuing on the same insulin regime. The patient was subsequently admitted to a general ward for further evaluation and management.

slovenia
by Rok Petrovčič from Slovenia.

A new chapter from Shabana Walia

Thyroid Storm chapter written by Shabana Walia from USA is just uploaded to the Website!

38 - atrial fibrillation

A 68-year-old female with hypertension presented to the emergency department with worsening of lower extremity swelling for the last few months. She appeared to be confused over the last three days according to her husband. He also noted that she had a fever. She had intermittent chest discomfort and was feeling “anxious.” She was compliant with the prescribed antihypertensive (lisinopril and hydrochlorothiazide). She used no tobacco or illicit drug. She had a family history of hypertension and hyperthyroidism.

Her vitals at triage were as follows: BP 170 over 86mmHg, HR 136/min, RR 18/min, Temperature 40.2°C and SP O2 100% on room air. She appeared agitated and flushed, with bilateral exophthalmos and lid lag. Her thyroid was diffusely enlarged with bruit noted. Her pulse was irregularly irregular. She had pitting edema up to the mid-shin. Bilateral plantar reflexes were 3+. The rest of the physical examination was unremarkable.

Her blood test results were as follow:
Normal CBC and renal function.
Calcium: 11.5 mg/dL
Thyroid stimulating hormone (TSH) < 0.01 milli-international unit/L
Free T3: > 30 picogram/mL
Free T4: > 6 nanogram/dL
Troponin: 0.1
Pro-BNP: 3,000 picogram/mL

A diagnosis of hyperthyroidism was made, and she was evaluated for possible thyroid storm.

by Shabana Walia from USA.

A new chapter

Hyponatremia chapter written by Vigor Arva and Gregor Prosen from Slovenia is just uploaded to the Website!

Bohermeen Spring Half Marathon 2014

A 72-year-old man was brought to the emergency department by his daughter. She reported that he had nausea, vomiting, and confusion and had been unwell for the last few days. He had hypertension and heart failure for the previous ten years and was on ACE-inhibitor, beta-blocker and thiazide diuretic.

At triage, the patient’s vital signs were usual: blood pressure 110 over 70 mmHg, heart rate 95/min, respiratory 15/min, temperature 36.1°C and SpO2 100% on room air. He appeared lethargic and walked with an unsteady gait. He had no focal neurological deficit. He had a normal skin turgor and no edema. Postural BP revealed mild orthostatic hypotension. The lab results showed a serum sodium concentration of 115 mEq/L.

slovenia
by Vigor Arva and Gregor Prosen.

A comprehensive chapter from Toh Hong Chuen

Hyperglycemia chapter written by Toh Hong Chuen from Singapore is just uploaded to the Website!

61 - Diabetic Foot - Subcutaneous air

A 58-year-old lady presented with right foot pain for 3 days, associated with high fever, lethargy, polyuria, and polydipsia. At triage, air hunger was noted. Her vital signs were: blood pressure 82 / 46 mmHg, heart rate 131/min, respiratory rate 28/min, Temperature 38.7 and SpO2 98%. She was brought to the resuscitation room for further management.

Clinically, she was dehydrated and confused with GCS 14. Her neck was supple, and lungs were clear. Crepitus was noted on the dorsum of the right foot. Point of care blood tests showed: capillary glucose 40 mmol/L, capillary ketone 7.2 mmol/L, pH 7.22, bicarbonate 8 mmol/L, pCO2 20 mmHg, sodium 130 mmol/L, chloride 95 mmol/L, potassium 5.5 mmol/L and lactate 6.9 mmol/L.

A diagnosis of septic shock secondary to gas gangrene complicated by diabetic ketoacidosis was made. She was aggressively resuscitated with fluid and started on I.V. insulin infusion. Potassium replacement was withheld as potassium was elevated. Urinary catheterization was performed for strict input-output monitoring. Broad-spectrum antibiotics and intramuscular tetanus toxoid were given. X-ray of right foot confirmed subcutaneous air.

The patient was sent directly to the theatre and underwent extensive debridement for the gas gangrene. She had an uneventful recovery and was discharged 1 week later.

by Toh Hong Chuen from Singapore.

Do you have 9 minutes 40 seconds?

Hypernatremia chapter written by Vigor Arva and Gregor Prosen from Slovenia is just uploaded to the Website!

Pink Salt ^w^

A 79-year-old man was brought to the emergency department (ED) by his wife. She complained that the patient had general weakness and was feeling ‘unwell’ for the last two days. He had a history of dementia, diabetes, renal failure, and hypertension. He was on diabetic and antihypertensive medication.

On examination, his vital signs were as follow HR 115/min, BP 135/90 mmHg, RR 17/min, and afebrile with normal oxygen saturation. He was confused and disoriented, but there was no other deficits or localizing signs on neurological exam. He was clinically dehydrated with dry oral mucosa. Lab results showed a serum sodium concentration of 160 mEq/L, with elevated glucose, creatinine, urea, and osmolality. Point of care ultrasound demonstrated a small and almost totally-collapsed inferior vena cava. Upon further history taking, the patient’s wife reported that he had not been drinking much for the last few days, even though he did not complain about thirst.

slovenia
by Vigor Arva and Gregor Prosen from Slovenia