Category: Endocrine and Electrolyte Emergencies

Hypernatremia (2024)

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by Theresa Nguyen

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You Have A New Patient!

An 87-year-old male patient with a past medical history of hypertension, stroke, and depression presents to the ED with lethargy and altered mental status. He was brought in by his daughter, who states that she has been visiting him at the nursing home over the past three days, during which he has appeared progressively weaker and more confused. 

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The nursing home staff report that the patient has had poor oral intake and multiple episodes of non-bloody diarrhea. He has not been participating in his usual activities and appeared more lethargic today, which prompted his daughter to bring him to the ED.

Initial triage vital signs are as follows: BP 92/60, HR 134, RR 18, SpO₂ 99%, Temp 36.8°C.

Exam findings are notable for a cachectic elderly male who is not oriented to person or place. He appears clinically dehydrated, with dry mucous membranes and poor skin turgor with tenting. He is able to follow basic commands but appears weak and confused. Laboratory findings were notable for a sodium of 165 mEq/L, chloride of 120 mEq/L, potassium of 4.0 mEq/L, and creatinine of 2.1 mg/dL.

What is the diagnosis for this patient, and what additional labs, treatment options, and potential complications should be considered?

What Do You Need To Know?

Importance and Epidemiology

Hypernatremia is defined as a serum sodium ([Na+]) level greater than 145 mEq/L [1]. It is a common electrolyte abnormality seen in elderly, pediatric, and critically ill patients, as these populations are more prone to impaired thirst regulation [2]. Hypernatremia occurs due to net water loss, excess sodium intake, or a combination of both [1]. Accurate diagnosis and appropriate treatment are crucial, as both undercorrection and overcorrection of hypernatremia are associated with poor prognosis and a high mortality rate of 40–60%, which is often underappreciated [1].

Pathophysiology

Understanding hypernatremia requires comprehension of the main body fluid compartments as well as the basic concepts of normal body water balance [1]. Since sodium is important for maintaining extracellular fluid (ECF) volume, any change in ECF volume can result in increased or decreased sodium excretion in the urine. Sodium excretion is regulated by mechanisms such as the renin-angiotensin-aldosterone system [1]. When there is a rise in serum sodium, plasma osmolality also increases, triggering the thirst response and antidiuretic hormone (ADH) secretion. This leads to renal water conservation and the production of concentrated urine [1].

Severe hypernatremia occurs when serum sodium rises rapidly or exceeds 160 mEq/L [2]. Most patients will be symptomatic at this level due to central nervous system dysfunction. Hypovolemic hypernatremia is the most common presentation of hypernatremia seen in the ED, as net water loss accounts for the majority of cases [3]. Determining the patient’s volume status is one of the most important steps in managing hypernatremia. A thorough history, clinical exam, and laboratory testing are used in conjunction to establish the etiology of hypernatremia.

Medical History

As stated previously, a thorough history is essential to determining a potential etiology for hypernatremia and guiding management [1]. For example, patients who have sustained a traumatic brain injury may be more likely to have central diabetes insipidus (DI), while a patient with an underlying psychiatric condition on lithium may be more likely to have nephrogenic DI [1]. The timing of symptoms is also relevant in determining whether the hypernatremia is acute or chronic. Hypernatremia that develops within the previous 48 hours is considered acute, while patients with symptoms lasting longer than 48 hours or with unknown timing of symptom onset are considered to have chronic hypernatremia [1]. The severity of symptoms is determined by both the speed and magnitude of the Na+ change.

The history should include detailed information about the patient’s fluid and salt intake, urine output, past medical history, and current medications [4]. Medications often implicated in hypernatremia include loop diuretics, lithium, phenytoin, lactulose, aminoglycosides, mannitol, and hypertonic saline [3,5]. Ask about any recent head trauma or surgeries, such as pituitary macroadenoma removal. Patients may report polyuria, polydipsia, confusion, or generalized weakness. If the patient is altered, the caregiver or family member (if available) should be interviewed to determine any specific mental or behavioral changes that are acute.

Physical Examination

Assess the patient’s volume status by checking skin turgor and capillary refill, in addition to examining for edema or elevated jugular venous pressure [1]. Vital sign abnormalities may include tachycardia or orthostatic hypotension. Check for signs of trauma, burns, infection, or skin breakdown, which may contribute to insensible water losses.

Patients with underlying hypernatremia may present with a broad range of signs and symptoms, including lethargy, irritability, restlessness, altered mental status, poor skin turgor, hyperactive reflexes, and increased muscle tone [5]. Hypovolemic patients are usually tachycardic, with decreased capillary refill and peripheral perfusion, while hypervolemic patients may appear edematous and have rales on exam.

Perform a complete neurologic exam on all patients presenting with hypernatremia, as altered mental status, seizures, and a comatose state are associated with greater risk of morbidity and mortality [5]. Cerebral adaptation to hypernatremia generally starts on the first day and results in a reduction of brain volume that is reversed by water movement from the cerebrospinal fluid into the brain [1].

Check for somnolence, disorientation, increased muscle tone, or spasticity. Patients may often appear weak and lethargic.

Classifications of Hypernatremia & Alternative Diagnoses

Following the initial history and assessment as detailed above, patients with hypernatremia can be categorized into one of the following three groups depending on their volume status.

Hypovolemic Hypernatremia (Concomitant Loss of Water and Salt):

Patients with hypovolemic hypernatremia experience both a loss of water and salt, but with a relatively larger loss of total body water (TBW) [1]. This is most commonly due to gastrointestinal losses (e.g., diarrhea, vomiting), skin losses (e.g., burns or excessive sweating), and renal losses (e.g., intrinsic renal disease, mannitol, and loop diuretics) [5].

Patients with hypovolemic hypernatremia should first be given normal saline solution or lactated Ringer’s to restore volume, followed by hypotonic saline solutions (e.g., half-isotonic saline or quarter-isotonic saline). Hypovolemic hypernatremia is the most common presentation of hypernatremia seen in the ED [3].

Euvolemic Hypernatremia (Water Loss with Normal Salt Content):

This results from decreased TBW without any accompanying loss of salt [1]. Euvolemic hypernatremia is caused by extrarenal losses from the respiratory tract or skin (e.g., excessive sweating or fever), renal losses (e.g., central diabetes insipidus [DI] or nephrogenic DI), and other causes such as medications [5].

Medications often associated with euvolemic hypernatremia include lithium, amphotericin, phenytoin, and aminoglycosides [3,5]. Treatment for euvolemic hypernatremia is aimed at free water replacement, which can be provided orally or through intravenous glucose solution.

Diabetes Insipidus (DI): Also known as arginine vasopressin deficiency (AVP-D), DI is characterized by the passage of large volumes (>3 L/24 hours) of dilute urine [6]. The classic presentation of DI in the ED includes symptomatic hypernatremia (e.g., polyuria, polydipsia, lethargy, and weakness) and an inappropriately low urine osmolality (<300 mOsm/kg) [6].

DI refers to an absolute or relative antidiuretic hormone (ADH) deficiency and can be further classified into two major forms:

  • Central DI: Characterized by an absolute ADH deficiency caused by inadequate ADH secretion. Common etiologies include malignant diseases, head trauma, pituitary surgery, infiltrative diseases, or idiopathic conditions [6].
  • Nephrogenic DI: Characterized by a relative ADH deficiency due to a lack of renal response to ADH. Common etiologies include chronic renal insufficiency, polycystic kidney disease, hypercalcemia, hypokalemia, lithium toxicity, or familial diseases [6].

Hypervolemic Hypernatremia (Relative Water Deficit with Concomitant Gain in Salt):

This less common form of hypernatremia results from increased sodium with normal or increased TBW [1]. Hypervolemic hypernatremia often has an iatrogenic cause, such as hypertonic fluid administration (e.g., hypertonic saline, sodium bicarbonate, or total parenteral nutrition) in hospitalized patients [1]. It can also result from ingestion of saltwater or large amounts of salt, as well as mineralocorticoid excess (e.g., adrenal tumors or congenital adrenal hyperplasia) [4].

Patients with hypervolemic hypernatremia will often appear volume overloaded. Many of these patients may have conditions contributing to salt retention, such as congestive heart failure, liver dysfunction, renal disease, or hypoalbuminemia [1]. Treatment involves free water replacement and the use of diuretics such as furosemide to promote sodium excretion [4]. Diuretics should be titrated as necessary to maintain a negative fluid balance [3].

Acing Diagnostic Testing

Laboratory testing is another essential component for determining the causative factors of hypernatremia, especially in patients with altered mental status who cannot provide a thorough history [1]. Obtain a full set of serum electrolytes (including magnesium, calcium, and phosphate), liver function tests, renal function tests, urine electrolytes, and calculate serum osmolality. A serum osmolality of >430 mOsm/L is often associated with seizures and death [5].

The urine osmolality is one of the most useful initial tests to order, as it can further categorize the etiology and determine whether or not the renal water-concentrating ability is preserved [1]. If the urine osmolality is less than 300 mOsm/kg, this favors a diagnosis of central or nephrogenic DI. Desmopressin (DDAVP) should be administered to differentiate between the two types of DI. In patients with central DI, DDAVP will result in an increase in urine osmolality [1,6]. If the urine osmolality is high (greater than 800 mOsm/kg), this suggests that the secretion and response to AVP are normal, indicating preserved renal concentrating ability. In such cases, the hypernatremia is most likely due to extrarenal losses [1].

Imaging can also be useful in determining other etiologies of hypernatremia and ruling out potentially life-threatening conditions. Obtain a chest x-ray to rule out congestive heart failure, pneumonia, malignancy, pulmonary edema, and cardiomegaly as potential contributing disease processes. A non-contrast CT scan of the head is recommended in all patients with severe hypernatremia, especially if focal neurologic findings are present on exam. Hypernatremia results in traction on dural bridging veins and sinuses, which can lead to intracranial hemorrhage, most often in the subdural space [3]. Hemoconcentration from total body water loss may also lead to dural sinus thrombosis.

Risk Stratification

As mentioned previously, the severity of symptoms is often determined by both the speed and magnitude of the Na+ change. Acute symptoms are usually noted when Na+ >160 mEq/L [2]. Patients with acute hypernatremia are more likely to present with neurologic manifestations such as confusion, altered mental status, seizures, or ataxia. In cases of rapid and severe hypernatremia that develops over minutes to hours, there is an increased risk of acute intracranial hemorrhage due to the accompanying rapid decrease in brain volume, which causes rupture of cerebral veins [3].

Patients with chronic hypernatremia are typically less likely to exhibit neurologic symptoms due to the brain’s compensatory mechanisms. The brain can adapt by generating intracellular osmogenic compounds, which increase osmolality in the cells and thereby maintain brain volume, resisting shrinkage [1].

Management

The ED management of hypernatremia revolves around two key tasks: treating the inciting cause and correcting the hyperosmolality [1,3]. It is important to note that correcting sodium either too quickly or too slowly is associated with an increased risk of death and cerebral edema [3]. Therefore, the treatment of hypernatremia requires appropriate timing and a systematic approach. The classic recommendation for the management of hypernatremia is to replace the calculated free water deficit over 48 hours, with a decrease in serum Na+ not to exceed 0.5 mEq per hour (or 10–12 mEq total per 24 hours) [2,7].

ED management of hypernatremia can be further broken down into the following steps:

1) Resuscitate:

Following the initial evaluation, patients who are hemodynamically unstable should be resuscitated with intravenous fluids to stabilize abnormal vital signs [7]. The initial goal is to address the underlying hypovolemia and tissue hypoperfusion. Unless this is corrected, the body’s normal response will be to increase sodium concentration to maintain intravascular volume, which will worsen hypernatremia. Fluid resuscitation can be initiated with an isotonic fluid such as normal saline (0.9%) or lactated Ringer’s for volume repletion [2].

While it may seem counterproductive to administer a sodium-containing fluid to a hypernatremic patient, the goal is to restore homeostatic mechanisms of sodium balance before free water correction [2]. If the patient is not hypovolemic, use D5W for fluid resuscitation.

2) Investigate:

Evaluate for and treat the underlying cause of hypernatremia [2,7]. Review the patient’s weight, intake and output, and current medications. Consider potential etiologies of hypernatremia, such as electrolyte imbalances, gastrointestinal losses, diabetes insipidus, and others as described above. Look for potential sources of infection.

Obtain additional labs to help identify the etiology of hypernatremia and direct management. Rule out other electrolyte abnormalities, such as hypokalemia and hypercalcemia, which may point to renal causes of hypernatremia [3]. Calculate the serum osmolality (normal reference range: 275–295 mOsm/L), as elevations may correlate with the degree of symptoms [5]. Once the cause of hypernatremia has been identified, treat the underlying condition.

3) Rehydrate:

Water replacement should address the total body water (TBW) deficit in addition to any ongoing losses of water. Each liter of water deficit raises the serum Na+ by approximately 3–5 mEq/L [1]. Calculate the free water required to achieve the target sodium level [7]. The choice of replacement solution and infusion rates are critical factors to avoid overcorrection of hypernatremia.

It is essential to know the sodium concentration in different solutions to accurately correct water and sodium imbalances [3]. The sodium concentrations in commonly used solutions are listed below [3]:

  • 0.9% NaCl: 154 mmol/L
  • Ringer’s Lactate: 130 mmol/L
  • 0.45% NaCl: 77 mmol/L
  • 5% Dextrose in water (D5W): 0 mmol/L

To determine the TBW and water deficit:

  1. Calculate TBW:
    The total body water (TBW) is estimated as 50% or 60% of lean body weight in women and men, respectively, which is why different correction factors are used in TBW calculation. Below are the recommended correction factors for calculating TBW based on age and gender [7]:
  • Children and adult males: 0.6 × weight (kg)
  • Adult females: 0.5 × weight (kg)
  • Elderly males: 0.5 × weight (kg)
  • Elderly females: 0.45 × weight (kg)
  1. Calculate water deficit:
    The water deficit as a function of sodium concentration is calculated using the formula [1,3]:
    TBW deficit = TBW × [(serum sodium/140) – 1]

This equation approximates the amount of water required to decrease sodium concentration to 140 mEq/L [3]. Note that this equation does not account for ongoing water losses or coexisting isosmotic fluid deficits, such as in patients with ongoing vomiting or diarrhea.

Rate and Volume of Correction:

Once the water deficit has been calculated, determine the rate and volume of correction. Several free online calculators, such as those available on MedCalc, can be used as reference tools.

  • Acute hypernatremia: Do not lower sodium by more than 1–2 mEq/L/hr.
  • Chronic hypernatremia: The goal is to lower Na+ by 10–12 mEq over 24 hours [5].

Avoid rapid overcorrection of hypernatremia, as this can result in cerebral edema, especially in children, who are more prone to this complication. Many patients with hypernatremia will also have reduced extracellular fluid (ECF) volume and other electrolyte abnormalities, which may require hypotonic fluids.

Treatment of Central DI:

The main treatment modality for patients with central DI is to supplement ADH in the form of desmopressin (DDAVP) [1]. Patients with known central DI should be given desmopressin, which may improve symptoms.

The initial dose of DDAVP is 1–2 micrograms (administered orally, intranasally, subcutaneously, or intravenously) and then up-titrated as necessary to reach the goal sodium level [6].

Special Patient Groups

Pediatrics

Hypernatremia is predominantly seen in infants and the elderly population due to their impaired thirst regulation [1]. Infants and small children are more vulnerable to hypernatremia because of their greater insensible water losses and their inability to communicate their need for fluids and/or access fluids independently. Two common presentations for infants at risk of hypernatremia include those receiving inadequate hydration in the setting of gastroenteritis or ineffective breastfeeding [2]. Furthermore, premature infants are at higher risk due to their relatively small mass-to-surface area ratio and their dependency on caregivers for fluid intake [2].

In breastfed infants, a relevant history should focus on whether there is a successful latch at the start of breastfeeding, the frequency and duration of feedings, the mother’s sensation of milk letdown, and whether the infant appears satiated after feeding. Common symptoms of hypernatremia in infants may include lethargy, weakness, restlessness or agitation, and a characteristic high-pitched cry [3]. It is important to remember that the degree of dehydration can be underestimated in children with hypernatremia due to a shift of water from the intracellular space to the extravascular space [2]. Children are often more susceptible to adverse effects from rapid correction of hypernatremia.

Pregnant Patients

Pregnant patients may develop hypernatremia due to transient diabetes insipidus, which affects approximately 4 out of 100,000 pregnancies [6]. Between the eighth gestational week and midpregnancy, the metabolic clearance of ADH increases 4- to 6-fold because of an increase in the enzyme vasopressinase, which is produced by the placenta. Vasopressinase activity peaks in the third trimester, remains high during labor and delivery, and then falls to undetectable levels two to four weeks postpartum [6]. Transient DI is caused by an amplification of the normal pregnancy-related increase in vasopressinase levels. Patients generally report increased thirst and urinary output that are out of proportion to those normally seen in pregnancy.

Patients with preeclampsia or HELLP syndrome are at increased risk for transient DI of pregnancy [8]. Transient DI should also be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after a Caesarean section [8]. Treatment options for transient DI of pregnancy include desmopressin and free water replacement [6]. Transient DI typically resolves postpartum and does not usually recur in subsequent pregnancies.

Geriatrics

Hypernatremia is also a relatively common electrolyte disorder in the elderly and critically ill patients. Approximately 27% of patients admitted to an intensive care unit (ICU) develop hypernatremia of variable severity during their ICU stay [9]. Additionally, studies have found that hypernatremia is an independent predictor of mortality and length of stay after controlling for illness severity and other ICU-acquired conditions and complications [9]. Even mild hypernatremia, with serum sodium levels between 145 and 149 mEq/L, is associated with a 28% increase in mortality risk and a 19% increase in ICU length of stay [9].

In the elderly population, the causes of hypernatremia tend to be multifactorial and include a decrease in thirst sensation, polypharmacy, and pre-existing comorbidities [10]. Renal function, concentrating abilities, and hormonal modulators of salt and water balance are often impaired in the elderly, making them more susceptible to hypernatremia and the associated morbidities and iatrogenic events involving salt and water [10]. The age-related decrease in TBW and concomitant impairment in thirst mechanisms also make elderly individuals more vulnerable to stresses on water balance [10]. By age 75 to 80 years, total body water content declines to approximately 50%, and even lower in elderly women. Providers should maintain a high index of suspicion for hypernatremia in elderly patients presenting from long-term care facilities, nursing homes, or after prolonged inpatient hospitalizations.

When To Admit This Patient

Patients with symptomatic hypernatremia or a serum sodium level greater than 150 mEq/L should be admitted to the hospital for further evaluation and treatment, as the free water deficit will generally need to be replaced gradually [1]. Those with severe neurological symptoms should be admitted to the ICU for regular neurologic exams. If available, a nephrology consult may be required for recommendations on dialysis and fluid regimens in more severe cases of hypernatremia. Sodium and electrolyte levels should be closely monitored every 2 to 4 hours during the acute phase of correction [2]. If a patient develops seizures during the course of treatment, this may indicate cerebral edema caused by rapid shifts in osmolality [2].

Hemodynamically stable and asymptomatic patients with mild hypernatremia from benign causes may be discharged with outpatient follow-up. Any medications contributing to the hypernatremia should be appropriately tapered or discontinued. Patients should be given specific instructions on the appropriate daily fluid intake and advised to avoid foods high in sodium (such as soy sauce, canned soups, chips, and processed foods) [1]. A plan should be in place to obtain follow-up sodium levels within 5 to 7 days or sooner if the patient becomes symptomatic.

Patients should also be instructed to return for any worsening fatigue, altered mental status, increased thirst, or confusion. Serum sodium and drug levels should be periodically monitored in patients taking medications known to cause nephrogenic DI. For elderly patients, a coordinated discharge plan involving the discharging physician, primary care physician, and nursing home staff is essential to prevent readmission due to hypernatremia [2].

Revisiting Your Patient

This case presents a common scenario where an elderly nursing home resident with poor oral intake presents to the ED with altered mental status and lethargy due to decreased oral intake and diarrhea. Vital signs are notable for tachycardia and hypotension, along with physical exam findings of dry mucous membranes and poor skin turgor. The patient was found to be hypernatremic, with a sodium level of 165 mEq/L and an elevated creatinine of 2.1 mg/dL. These findings are consistent with a clinical picture of hypovolemic hypernatremia.

Additional history obtained from the patient’s daughter and a review of nursing home records revealed medications that included lisinopril, aspirin, and sertraline. There were no recent medication changes, and the patient was still taking all of his medications despite the reported decrease in oral intake. Regarding his baseline mental status, the patient is typically communicative and usually awake, alert, and oriented to person, place, and time. He is now more confused and only oriented to person. There was no reported trauma or recent surgeries.

The patient was initially fluid resuscitated with 1 L of normal saline to stabilize the tachycardia and hypotension. Given the change in mental status, a head CT was performed, which did not show any acute intracranial hemorrhage or brain mass. A chest x-ray revealed no acute cardiac disease, focal consolidation, or pulmonary edema. Additional labs did not reveal any other electrolyte abnormalities. His serum osmolality was calculated to be 352 mOsm/kg, and his urine osmolality was elevated at >800 mOsm/kg.

Following initial fluid resuscitation, the patient’s calculated water deficit was estimated to be 5.35 L using the formula:
TBW deficit = TBW × [(serum sodium/140) – 1]
Using a weight of 60 kg:
(0.5 × 60 kg) × [(165/140) – 1] = 30 × (1.18 – 1) = 5.35 L

Given the patient’s altered mental status, degree of dehydration, and significant hypernatremia, he was admitted to the hospital for additional monitoring and fluid management. His IV fluids were adjusted to achieve a goal of decreasing the Na+ by 0.5 mmol/L/hr.

The patient responded well to treatment, and his confusion gradually resolved. He was discharged back to the nursing home within 3 days and did not experience any adverse outcomes.

Author

Picture of Theresa Nguyen

Theresa Nguyen

Dr. Theresa Nguyen is an Associate Professor of Emergency Medicine and the Director of the Center for Community and Global Health at Loyola University Medical Center in Maywood, IL. She also co-founded the Loyola Street Medicine program, which is dedicated to providing medical care and social outreach to individuals experiencing homelessness. Dr. Nguyen has international fieldwork experience in Haiti, Peru, Guatemala, Dominican Republic and Vietnam. Over the course of her global health work, Dr. Nguyen developed a strong interest in tropical diseases and obtained her Certificate of Knowledge in Clinical Tropical Medicine and Travelers' Health in 2014. Dr. Nguyen's current interests include ultrasound teaching in resource-limited settings, addressing language barriers, providing access to care for the homeless population, increasing awareness and education surrounding human trafficking, and international EM development.

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References

  1. Muhsin SA, Mount DB. Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab. 2016;30(2):189-203.
  2. Sonani B, Naganathan S, Al-Dhahir M. Hypernatremia. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2023. Updated May 20, 2023. Accessed June 19, 2023. https://www.ncbi.nlm.nih.gov/books/NBK441960/
  3. Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493-1499.
  4. Farkas J. Hypernatremia and dehydration in the ICU. The Internet Book of Critical Care. Published June 25, 2021. Accessed April 3, 2023. https://emcrit.org/ibcc/hypernatremia/
  5. Liamis G, Filippatos TD, Elisaf M. Evaluation and treatment of hypernatremia: a practical guide for physicians. Postgrad Med. 2016;128(3):299-306.
  6. Hui C, Khan M, et al. Diabetes Insipidus. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2023. Updated June 1, 2023. Accessed June 19, 2023. https://www.ncbi.nlm.nih.gov/books/NBK470458/
  7. Ramzy MM. EM@3AM: Hypernatremia. emDocs. Published July 14, 2018. Accessed April 10, 2023. https://www.emdocs.net/em3am-hypernatremia/
  8. Sherer DM, Cutler J, Santoso P, et al. Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy. Obstet Gynecol. 2003;102(5):1166-1168.
  9. Chand R, Chand R, Goldfarb DS. Hypernatremia in the intensive care unit. Curr Opin Nephrol Hypertens. 2022;31(2):199-204.
  10. Kugler JP, Hustead J. Hyponatremia and hypernatremia in the elderly. Am Fam Physician. 2000;61(12):3623-3630.

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.

Hypoglycemia (2024)

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by Rok Petrovčič

 

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You Have A New Patient!

A 75-year-old woman was brought to the emergency department by her relatives for “not being her usual self” for the past day. Her relatives reported that the patient had not eaten much of her usual breakfast, as she was not feeling well. She was on insulin therapy for diabetes but was otherwise healthy, with no reported allergies. At triage, she appeared confused and disoriented. Her vital signs were as follows: HR 95/min, RR 18/min, BP 141/85 mmHg, T 37.7°C, and SpO₂ 99% on room air. 

The image was produced by using ideogram 2.0

Given her past medical history, a capillary blood glucose test was performed at triage, which revealed a reading of 2.6 mmol/L (47 mg/dL). She was laid down and brought to an examination room on a stretcher.

What Do You Need To Know?

Importance

Hypoglycemia is a common medical emergency that is easily treatable but can be life-threatening if not addressed promptly. It is a frequent condition in patients with diabetes. Hypoglycemia can cause a variety of symptoms, including confusion, loss of consciousness, seizures, and even coma. These symptoms can be mistaken for other conditions, so it is important to recognize the signs of hypoglycemia and provide prompt treatment. Hypoglycemia can often be treated with oral glucose, but severe cases may require intravenous administration of glucose or other medications. Knowledge of appropriate treatments for hypoglycemia is crucial to prevent serious complications. Hypoglycemia may also occur in patients with other conditions, such as liver failure or sepsis. In these cases, it is also important to address the underlying condition [1].

Epidemiology

The epidemiology and incidence of hypoglycemia are difficult to study, as many patients experiencing hypoglycemic symptoms recognize and treat them without visiting the emergency department (ED). Hypoglycemia is more common in patients with type 1 diabetes and less common in those with type 2 diabetes, due to therapies that less frequently induce hypoglycemia. In the United States, hypoglycemic events contribute to 100,000 emergency department visits annually, costing $120 million [2].

Pathophysiology

Glucose is the main source of energy, and its lack causes the release of glucagon, catecholamines, and growth hormone, leading to adrenergic symptoms. Hypoglycemia can be iatrogenic or secondary to an underlying disease process. Common causes of hypoglycemia in diabetic patients include medication (increased medication intake or decreased oral intake), infection, and worsening kidney function. In non-diabetic patients, common causes include infection, liver disease, and malignancy. Other causes in both groups of patients include Addison disease, adrenal crisis, cardiogenic shock, hypopituitarism (panhypopituitarism), inadequate intake of food, insulinoma, poisoning, stress, and suicide attempts involving anti-diabetic agents [1,3].

Medical History

Taking a thorough history in a hypoglycemic patient is critical for determining the etiology and guiding appropriate management. Below are key elements to address during history-taking:

1. Dietary History

Ask the patient about the timing, content, and size of their last meal. Skipping meals or consuming inadequate carbohydrates can precipitate hypoglycemia, particularly in individuals on glucose-lowering therapies. Recent fasting, changes in eating patterns, or prolonged periods without food (e.g., due to illness or dietary restrictions) should also be noted.

2. Physical Activity

Inquire about recent exercise or physical exertion. Increased physical activity, particularly without appropriate adjustments in food intake or medication, can lead to hypoglycemia. This is especially relevant for individuals on insulin or insulin secretagogues such as sulfonylureas [3].

3. Alcohol Use

Assess the patient’s alcohol consumption, including the amount and timing. Alcohol impairs gluconeogenesis in the liver and can precipitate hypoglycemia, particularly in individuals who have not eaten or who are on glucose-lowering medications.

4. Medication History

For patients with diabetes, a detailed review of their diabetic medication regimen is essential. Obtain information about the specific drugs used (e.g., insulins—categorized as rapid-, short-, intermediate-, or long-acting—or sulfonylureas), doses, and timing of administration. Missing meals or using incorrect dosages are common contributors to hypoglycemia in this population [4]. Additionally, check for the use of other medications that may potentiate hypoglycemia, such as beta-blockers or quinolone antibiotics.

5. Symptoms of Infection or Ischemia

Infections and ischemic conditions can exacerbate hypoglycemia by increasing metabolic demand or altering medication effects. Ask about recent fever, chills, cough, dysuria, chest pain, or other signs and symptoms that could indicate an underlying infection or ischemic event.

6. Drug Overdose or Intentional Harm

In cases of suspected hypoglycemia secondary to drug overdose, particularly with oral hypoglycemic agents like sulfonylureas, inquire about potential intentional overdoses or suicidal ideation. A suicide risk assessment must be conducted in these situations, as hypoglycemia from overdose can be life-threatening [3,4].

7. Family or Social History

If the patient is unable to provide a history, gather collateral information from family members, caregivers, or emergency medical personnel. This can help identify risk factors, such as undiagnosed diabetes or recent changes in behavior or treatment.

Physical Examination

A thorough physical examination is essential for evaluating a hypoglycemic patient and identifying the severity and potential underlying causes of their condition.

1. Initial Assessment

In any patient presenting with coma, altered behavior, or neurological symptoms, hypoglycemia must be considered and excluded early. Immediate bedside glucose measurement is critical to avoid delays in diagnosis and treatment. Early recognition and intervention can prevent irreversible neurological damage.

2. Signs of Neuroglycopenia

Neuroglycopenic symptoms arise from insufficient glucose supply to the central nervous system (CNS). Carefully assess for:

  • Level of Consciousness: Evaluate for confusion, lethargy, or unresponsiveness, which may range from mild cognitive impairment to profound coma. The Glasgow Coma Scale (GCS) can quantify the severity of neurological dysfunction.
  • Focal Neurological Signs: Perform a focused neurological examination for signs such as hemiparesis or cranial nerve deficits, which may mimic stroke and complicate diagnosis. The resolution of these signs with glucose administration supports hypoglycemia as the cause.
  • Seizure Activity: Look for evidence of tonic-clonic movements or postictal states, as seizures may be caused by severe hypoglycemia.
  • Ophthalmological Signs: Check for blurred vision or nystagmus, which may indicate neuroglycopenic involvement.

3. Adrenergic Signs

Adrenergic symptoms are the body’s compensatory response to hypoglycemia, mediated by catecholamine release. Key findings include:

  • Vital Signs: Look for tachycardia and tachypnea, which are nonspecific but often accompany adrenergic activation.
  • Skin Examination: Diaphoresis (profuse sweating) is a hallmark adrenergic response and can serve as a clinical clue.
  • Behavioral Symptoms: Assess for signs of agitation, restlessness, or pronounced anxiety, which may be linked to adrenergic stimulation.

The presence of adrenergic symptoms suggests an intact counter-regulatory response, whereas their absence in severe hypoglycemia may indicate an impaired sympathetic nervous system (e.g., in longstanding diabetes with autonomic neuropathy).

4. Whipple’s Triad

Whipple’s triad is critical for diagnosing hypoglycemia and should be confirmed whenever possible [3,4]:

  • Symptoms Consistent with Hypoglycemia: Correlate the findings of neuroglycopenic and adrenergic symptoms.
  • Low Blood Glucose Levels: Document with point-of-care testing or laboratory confirmation.
  • Resolution of Symptoms with Glucose Administration: Reassess the patient after treatment with glucose (e.g., oral glucose or IV dextrose). The resolution of symptoms reinforces the diagnosis.

5. Signs of Underlying Causes

Examine for evidence of potential precipitating conditions:

  • Infection: Check for fever, localized tenderness (e.g., chest, abdomen, or urinary tract), or signs of sepsis, as infections increase metabolic demand and can precipitate hypoglycemia.
  • Malnutrition: Assess for signs of cachexia or dehydration, which may indicate fasting or poor nutritional intake.
  • Drug Overdose: Look for clues such as medication vials, needle marks, or altered mental status in cases of suspected overdose with insulin or sulfonylureas.

6. Secondary Causes

Inquire about and examine for:

  • Adrenal Insufficiency: Hypotension, hyperpigmentation, and unexplained fatigue may point to Addison’s disease or secondary adrenal insufficiency.
  • Hypopituitarism: Look for evidence of chronic deficiencies such as hypotension, hypoglycemia, and bradycardia.

7. Systematic Re-Evaluation

The examination should be repeated after glucose administration to assess symptom resolution and identify any residual neurological deficits. Persistent focal findings or altered mental status post-treatment may indicate concurrent pathology, such as stroke or seizure disorder.

Alternative Diagnoses

If neurologic or behavioral symptoms persist after treatment with glucose, evaluate for concurrent causes of altered mental status using the mnemonic “TIPS AEIOU” [5]. A CT brain scan may be warranted.

  • A – Alcohol
  • E – Endocrine/Electrolyte/Epilepsy
  • I – Insulin
  • O – Overdose/Opioids/Oxygen
  • U – Uremia
  • T – Toxicologic/Trauma
  • I – Infection
  • P – Psychiatric/Poisoning
  • S – Stroke/Shock
ALTERED MENTAL STATUS

Acing Diagnostic Testing

A comprehensive diagnostic workup is crucial for identifying and addressing the cause of hypoglycemia while initiating timely treatment. 

1. Bedside Tests

Rapid bedside testing is the cornerstone for the initial evaluation of hypoglycemia:

  • Blood Glucose Measurement:
    Venous or capillary blood glucose should be checked immediately using a glucose oxidase strip. A glucose level <3.0 mmol/L confirms hypoglycemia. However, it is critical to remember that the severity of symptoms, rather than the absolute glucose value, determines clinical significance [3].
  • Point-of-Care Testing (POCT):
    Concurrent bedside tests such as arterial blood gas (ABG) analysis can provide information about acid-base status and potential coexisting conditions like sepsis or metabolic acidosis.

2. Laboratory Tests

Further laboratory investigations should be guided by the clinical presentation and differential diagnosis:

  • Formal Glucose Measurement:
    If hypoglycemia is detected on a bedside glucose test, a venous blood sample should be sent to the laboratory for a formal plasma glucose level. Importantly, treatment must not be delayed while awaiting these results.
  • Serum Insulin and C-Peptide:
    These are particularly useful when hypoglycemia secondary to endogenous hyperinsulinism or insulin overdose is suspected.
    • High Insulin and High C-Peptide: Suggest endogenous insulin production, as seen in insulinomas or sulfonylurea ingestion.
    • High Insulin and Low C-Peptide: Consistent with exogenous insulin administration [3].
  • Cortisol Levels:
    A low cortisol level may indicate adrenal insufficiency as a potential cause of recurrent hypoglycemia.
  • Glucagon Levels:
    Although not routinely assessed, glucagon levels can provide insights into counter-regulatory hormone responses during hypoglycemia.
  • Infection Markers:
    Full blood count, inflammatory markers (e.g., CRP, procalcitonin), and blood cultures should be obtained to investigate underlying sepsis or infection.
  • Toxicology Screen:
    Consider when an overdose of oral hypoglycemic agents or other substances is suspected.

3. Imaging Studies

Imaging is not routinely required for all patients with hypoglycemia but should be considered when specific conditions are suspected:

  • Chest X-Ray (CXR):
    Indicated if a respiratory infection or pulmonary source of sepsis is suspected.
  • Electrocardiogram (ECG):
    Perform in patients with suspected ischemia or when adrenergic symptoms such as tachycardia or chest pain are present.
  • Neuroimaging (CT or MRI):
    Obtain if the patient has persistent neurological symptoms after glucose correction or if there are signs of head trauma, stroke, or other CNS pathology.
  • Abdominal Ultrasound or CT Abdomen:
    Consider in cases of suspected pancreatic pathology, such as insulinoma or pancreatitis.

Key Considerations

  • There is no universally defined blood glucose threshold for hypoglycemia, as symptom onset varies among patients. Individual factors, such as baseline glucose control and underlying comorbidities, influence symptomatology [6].
  • Diagnostic tests should be tailored based on the clinical scenario to exclude critical conditions like infection, ischemia, or medication overdose. While advanced studies such as serum insulin and C-peptide are valuable, these are rarely performed in the emergency department and are more relevant in specialized or outpatient settings [3].

Risk Stratification

Factors to consider when risk stratifying patients with hypoglycemia include [3,7]:

  • Severity of hypoglycemia: Mild hypoglycemia can be managed by the patient with oral glucose or food, while severe hypoglycemia may require intravenous glucose and hospitalization.

  • Frequency of hypoglycemic episodes: Frequent hypoglycemic episodes can increase the risk of developing hypoglycemia unawareness, which may lead to more severe episodes in the future.

  • Underlying medical conditions: Patients with diabetes who have comorbidities, such as renal insufficiency or liver disease, may be at increased risk for hypoglycemia.

  • Age and cognitive function: Elderly patients or those with cognitive impairment may be at higher risk for hypoglycemia due to difficulty recognizing symptoms and managing their blood glucose levels.

  • Lifestyle factors: Patients with poor nutrition or irregular eating patterns may be at increased risk for hypoglycemia.

Management

Patients with hypoglycemia should be placed in a monitored area. If the patient has decreased consciousness or is unconscious, the airway should be protected, but intubation should be avoided prior to the administration of glucose. The means of reversing hypoglycemia depend on the patient’s mental status, ability to cooperate with oral intake, availability of intravenous access, and medical and medication history.

If the patient is conscious and able to cooperate with oral intake, administration of food or liquid rich in simple carbohydrates (e.g., a sugary drink, sugar, candies, or glucose tablets) is preferred. After this, the patient should receive a meal rich in complex carbohydrates, fat, and protein, such as a sandwich.

If the patient is unconscious or unable to cooperate with oral intake and intravenous access is available, administer 50 mL of IV dextrose 50% or 250 mL of 10% dextrose (equivalent to 25 g of dextrose) over a few minutes. A second dose can be administered if the patient’s mental status does not improve.

If intravenous access is not available, 1 mg of IM/SC glucagon can be administered. Glucagon takes longer to normalize mental status (approximately 7–10 minutes), and its effect tends to be short-lived. As glucagon raises blood glucose by mobilizing hepatic glycogen reserves, it is not effective in patients with depleted glycogen stores (e.g., liver failure or chronic alcoholism). Glucagon can also cause vomiting, which may be dangerous if the patient has an altered mental status and cannot protect their airway.

For patients with sulfonylurea overdose, commence therapy with IV dextrose until the patient can tolerate oral intake. If episodes of hypoglycemia recur despite glucose therapy, consider adding SC octreotide 50–100 micrograms. Note that octreotide should only be used for recurrent sulfonylurea-induced hypoglycemic episodes that persist despite glucose therapy [3,5].

Special Patient Groups

Pediatrics

Children are particularly vulnerable to the effects of hypoglycemia due to their higher metabolic rate and limited glycogen stores. Key points in management include:

  • Treatment Protocol:
    Administer 10% glucose at 5 mL/kg or 25% dextrose at 2.5 mL/kg intravenously for acute hypoglycemia. Avoid the use of 50% dextrose in this population, as its hypertonicity increases the risk of thrombophlebitis and local tissue injury [8].
  • Medication for Refractory Cases:
    For persistent hypoglycemia caused by hyperinsulinemia (e.g., from congenital hyperinsulinism or sulfonylurea overdose), octreotide is effective at a dosage of 1 μg/kg subcutaneously (maximum 50 μg). This medication inhibits insulin secretion and provides a targeted intervention [8].
  • Long-Term Considerations:
    Recurrent hypoglycemia in children warrants further investigation into metabolic or endocrine disorders, including inborn errors of metabolism, adrenal insufficiency, or insulinoma.

Pregnant Patients

Pregnant patients with diabetes, particularly those on insulin therapy, face a higher risk of hypoglycemia due to physiological changes during pregnancy, including increased insulin sensitivity in the first trimester.

  • Incidence:
    Up to 50% of pregnant patients with diabetes experience at least one episode of severe hypoglycemia during pregnancy, especially in the first trimester [4].
  • Management and Prevention:
    • Careful Insulin Titration: Frequent monitoring and adjustment of insulin doses are essential to balance optimal glycemic control with the prevention of hypoglycemia.
    • Dietary Counseling: Pregnant patients should be educated on consuming regular, balanced meals with adequate carbohydrate intake to prevent fasting hypoglycemia.
    • Monitoring: Emphasize regular blood glucose monitoring, as symptoms may be subtle or atypical.
  • Fetal Considerations: Prompt correction of maternal hypoglycemia is critical to prevent adverse effects on the fetus, including hypoxic injury from prolonged episodes.

Geriatrics

Older adults often experience atypical presentations of hypoglycemia, and their management is complicated by comorbidities, polypharmacy, and age-related physiological changes.

  • Atypical Presentations:
    Hypoglycemia in geriatric patients may lack typical adrenergic symptoms like tremors or sweating. Instead, symptoms such as confusion, lethargy, or falls may predominate, potentially delaying diagnosis.
  • Risk Factors:
    • Polypharmacy: Concurrent use of insulin, sulfonylureas, or other glucose-lowering agents increases hypoglycemia risk.
    • Renal Impairment: Reduced clearance of medications such as sulfonylureas or insulin exacerbates the risk of prolonged hypoglycemia.
    • Nutritional Deficits: Poor oral intake or prolonged fasting may contribute to hypoglycemia.

Intubated Patients

For intubated or sedated patients, hypoglycemia can be difficult to recognize because mental status changes are masked. In these cases, frequent glucose monitoring is essential [5].

When To Admit This Patient

Admission Criteria
Patients with hypoglycemia generally require admission to an observation unit or the general ward for evaluation and treatment of the underlying cause, as well as titration of diabetic medication.
Patients with unexplained or recurrent hypoglycemia should be admitted to a monitored area. Individuals taking sulfonylureas have an increased likelihood of experiencing recurrent and delayed-onset episodes of hypoglycemia. Consultation with a toxicologist and psychiatrist should be considered for patients who overdose on their diabetic medication [3,7].

Discharge Criteria
The patient should only be discharged if the cause of hypoglycemia is identified and deemed benign, they have fully recovered, are tolerating oral intake well, and have had no recurrence of hypoglycemic episodes after a 4-hour period of observation. Discharge advice should include guidance on nutrition and recognition of hypoglycemia symptoms. Patients should be advised to ingest glucose in case of symptoms [3].

Referral
If discharged from the ED, patients should be referred to their primary physician or specialist for follow-up. Patients should also be advised to always carry sugar or candy to ingest in case hypoglycemic symptoms arise [3].

Revisiting Your Patient

You examine your patient in the examination room. Upon examination, you notice a decreased level of consciousness, but otherwise, the exam is unremarkable. During the examination, the nurse obtains IV access and administers a bolus dose of intravenous glucose. Much to the relatives’ relief and amazement, the patient returned to her normal behavior within 5 minutes. The patient herself reported lower urinary tract symptoms with a low-grade fever over the last two days. The relatives also reported administering her insulin according to her daily regimen, without being cautious about her reduced food intake.

In addition, blood investigations revealed that her renal function had significantly deteriorated since her last primary care visit, despite continuing on the same insulin regimen. The patient was subsequently admitted to a general ward for further evaluation and management.

Recommended Free Open Access Medical Education (FOAM) resources

Author

Picture of Rok Petrovčič

Rok Petrovčič

Attending Physician - UKC Maribor / University Medical Centre Maribor

Listen to the chapter

References

  1. Mathew P, Thoppil D. Hypoglycemia. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2022. Updated July 23, 2022. Accessed February 24, 2023. https://www.ncbi.nlm.nih.gov/books/NBK534841/

  2. Maheswaran AB, Gimbar RP, Eisenberg Y, Lin J. Hypoglycemic events in the emergency department. Endocr Pract. 2022;28(4):372-377.

  3. Ravert D. Hypoglycemia. In: Mattu A, Swadron S, eds. CorePendium. Burbank, CA: CorePendium, LLC; 2021. Updated August 25, 2021. Accessed February 24, 2023. https://www.emrap.org/corependium/chapter/rec3z0v69Pks65AZg/Hypoglycemia#references

  4. Jalili M. Type 2 diabetes mellitus. In: Tintinalli JE, ed. Tintinalli’s Emergency Medicine. 7th ed. New York, NY: McGraw Hill; 2011:1431-1432.

  5. Nickson C. Hypoglycemia. In: Life in the Fast Lane. Accessed February 24, 2023. https://litfl.com/hypoglycemia/

  6. Frier BM. Defining hypoglycemia: what level has clinical relevance? Diabetologia. 2009;52(1):31-34.

  7. Oyer DS. The science of hypoglycemia in patients with diabetes. Curr Diabetes Rev. 2013;9(3):195-208.

  8. May N. Oh, sugar! Paediatric hypoglycaemia. In: St. Emlyn’s Blog. Accessed March 1, 2023. http://stemlynsblog.org/paediatric-hypoglycaemia/

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.

Gastroenteritis and Dehydration In Children (2024)

~ iEM Education Project Team ~ Leave a comment

by Neha Hudlikar & Abdulla Alhmoudi 

Authors
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You have a new patient!

14-month-old Zoey is brought to A&E by her mother with complaints of vomiting and diarrhea for one day. She has had six episodes of vomiting and eight episodes of loose stools since last night. She has also not had a wet diaper for almost 12 hours now. In triage, her vitals are HR 165 b/min, RR 45 br/min, Temperature 38.5 C, SpO2 97% CR 3 seconds. The nurse in triage notes that she has a glazed look. She is otherwise fit and well, with no past medical history. Zoey’s weight – 10 kg.

What will be your approach for this patient?

a-photo-of-a-baby (image produced by using ideogram2.0)

What do you need to know?

Importance

Acute gastroenteritis is one of the most common reasons for visits to pediatric emergency departments [1]. The World Health Organization (WHO) defines diarrhea as the passage of three or more liquid stools per day, or a more frequent passage than what is normal for the individual. When diarrhea occurs alongside vomiting, it is referred to as acute gastroenteritis (AGE).

Diarrhea can be categorized into three clinical types based on the presence or absence of blood and the timing of symptoms:

1. Acute watery diarrhea – lasts from hours to several days, but less than 14 days.
2. Acute bloody diarrhea – also known as dysentery, lasts less than 14 days.
3. Persistent diarrhea – lasts longer than 14 days.

Infectious gastroenteritis can be caused by various pathogens, including viruses, bacteria, and parasites. Rotavirus is the most common causative agent worldwide, responsible for 37% of diarrhea-related deaths in children under five years of age.

Epidemiology

Gastroenteritis is the second leading cause of death in children below the age of 5 and a leading cause of malnutrition in this age group. Globally, there are approximately 1.7 billion cases of childhood diarrheal diseases yearly, and the burden is substantial [2]. There is a direct impact of admission costs on the hospital budget and direct and indirect societal costs when children are admitted to hospitals.

In low-income countries, children under three years old, on average, have three episodes of diarrhea every year. This puts them at risk of malnutrition and, in turn, makes them vulnerable to further episodes of infectious diarrhea.

Pathophysiology

The loss of water and electrolytes via stools, vomit, sweat, and urine without adequate replacement leads to dehydration, a serious complication of gastroenteritis. Physiologic factors that predispose children to serious complications from dehydration include limited stores of fat and glycogen, relatively larger extracellular fluid compartments, and a limited ability to conserve water through their kidneys compared to adults.

Bicarbonate loss in stools, decreased tissue perfusion leading to anaerobic metabolism and lactic acid production, ketosis due to starvation, and decreased excretion of hydrogen ions due to poor renal perfusion are some of the mechanisms contributing to metabolic acidosis in pediatric dehydration due to acute gastroenteritis.

The exact pathophysiology depends on the causative agent. Infectious agents cause diarrhea via adherence, mucosal invasion, enterotoxin, and cytotoxin production.S. aureus and Bacillus cereus produce heat-stable enterotoxins in the food, which once consumed, lead to rapid onset of symptoms and are usually self-limiting. C. Perfingens, Enterotoxigenic E.coli produce enterotoxins in the small intestine leading to watery diarrhea. Other pathogens like enterohemorrhagic E. Coli (EHEC), Salmonella, Shigella, and Campylobacter jejuni produce toxins that directly invade the bowel leading to inflammatory diarrhea. Viruses often destroy the villus surface of the intestinal mucosa, and parasites often adhere to the mucosa.

Medical History

A focused and detailed history is essential to narrowing our differential diagnoses and guiding management. The history should include the timing, frequency, and severity of symptoms. We should also ask about any contact with someone with similar symptoms, known or suspected outbreaks in school or nursery, and recent travel.

All patients with acute gastroenteritis are at risk of dehydration, and the initial evaluation should include questions to assess its severity. The child’s oral intake, amount of urine passed, mental status (lethargy/irritability), etc., should be asked for in the initial evaluation. 

It is also important to ask for associated symptoms such as fever, abdominal pain, blood in the stools, and rash. Children with inflammatory diarrhea can develop serious illnesses like hemolytic uremic syndrome (HUS) with renal involvement. 

Other important questions in history include the child’s vaccination status, recent hospitalization/antibiotic use, and whether the child has any underlying chronic medical conditions/immunosuppression.

Physical Examination

Examining the child should be systematic, looking for the severity of dehydration and differentiating gastroenteritis from other causes of vomiting and diarrhea in children.

General examination should include the child’s appearance, alertness, lethargy, irritability, and weight. Vital signs should be assessed relative to the age. Physicians should look for explicit signs of dehydration, such as dry mucous membranes, sunken eyes, depressed fontanelle, and the presence/absence of tears. The cardiovascular exam should include heart rate, quality of pulses, and central and peripheral capillary refill times. Deep, acidotic breathing suggests severe dehydration. An abdominal examination assesses tenderness, bowel sounds, guarding, and rebound. Flank tenderness increases the likelihood of pyelonephritis. Examine the skin to check skin turgor, peripheral temperature, and other signs such as jaundice/rash.

Abnormal skin turgor, prolonged capillary refill time, and abnormal respiratory pattern are the three most useful examination findings in children with more than 5% dehydration [3]. It is important to note that these signs can be subtle, and determining the severity of dehydration accurately is challenging for physicians.

Alternative Diagnoses

Dehydration most commonly results from acute gastroenteritis in children. However, other diagnoses should be considered based on physical examination and history. Children with fever who are very ill-looking should have sepsis as one of the differential diagnoses. Other diagnoses to consider are urinary tract infection, appendicitis, hemolytic uremic syndrome, intussusception, and diabetic ketoacidosis. Symptoms immediately after ingestion should prompt physicians to consider ingestion of a foreign body or toxic substance. 

Vomiting and diarrhea are two important components that ED practitioners need a careful evaluation to rule in or out various diseases.

When evaluating vomiting in children, it is essential to consider a wide range of differential diagnoses spanning several systems. Central nervous system causes include space-occupying lesions, hydrocephalus, and infections. Cardiac-related vomiting may be attributed to congestive heart failure from various etiologies. Gastrointestinal conditions such as intussusception, midgut volvulus, pyloric stenosis, appendicitis, and esophageal or hepatic disorders are significant considerations. Renal issues like urinary tract infections, pyelonephritis, renal insufficiency, and renal tubular acidosis can also manifest as vomiting. Furthermore, metabolic and endocrine abnormalities, including diabetic ketoacidosis, Addisonian crisis, congenital adrenal hyperplasia, and inborn errors of metabolism, are key causes. Infectious conditions such as sepsis, pneumonia, otitis media, streptococcal pharyngitis, and gastroenteritis must also be included in the diagnostic workup.

Diarrhea in children can arise from diverse causes. Gastrointestinal disorders such as intussusception, Hirschsprung’s disease with toxic megacolon, inflammatory bowel disease, and appendicitis are prominent. Renal conditions, including urinary tract infections and pyelonephritis, can also lead to diarrhea. Infectious etiologies like sepsis, pneumonia, gastroenteritis, and pseudomembranous colitis are frequent contributors. Other causes include drug effects or overdose, hemolytic uremic syndrome, and congenital secretory diarrhea.

Understanding these potential causes is essential for accurate diagnosis and effective management.

Acing Diagnostic Testing

The workup should be guided by history and physical examination to determine the level of dehydration. In most cases, it is a self-limiting disease, and the principal goal of testing in ED should be to identify and correct fluid, electrolyte, and acid-base deficits. 

Most children with mild to moderate disease require no diagnostic testing. Children requiring IV hydration should have blood gas, serum electrolytes, bicarbonate, urea, and creatinine levels tested. It is common for young children to have hypoglycemia, and checking serum glucose levels is important. In children presenting with fever or mucous/blood in their stools, consider testing for fecal leucocytes to support a diagnosis of invasive diarrhea. A positive test should be followed by a stool culture, and it is important to note that a negative test does not rule out invasive disease.

Consider additional testing, such as blood and urine cultures, chest X-rays, and lumbar puncture, in immunosuppressed patients, infants less than 2 months old, or children with suspicion of bacteremia or localized invasive disease. 

Risk Stratification

The Gorelick scale and The Clinical Dehydration Score (CDS) are two of the most widely used scoring systems to predict the presence and severity of dehydration in the pediatric population. It is important to note that neither can definitively rule in or out dehydration in children and infants. Physicians should continue to use a structured approach to patients presenting with acute gastroenteritis and use these scores to aid clinical decision-making [4,5,6].

Clinical Dehydration Scale

 

0

1

2

 

0: No dehydration (<3%)

1-4: Some dehydration (≥3%- <6%)

5-8: Moderate dehydration (≥6%)

General appearance

Normal

Thirsty, restless or lethargic but irritable when touched

Drowsy, limp, or comatose

Eyes

Normal

Slightly sunken

Very sunken

Mucous membranes

Moist

“Sticky”

Dry

Tears

Present

Decreased

Absent

 

Gorelick Scale for Dehydration

characteristic

no or minimal dehydration

moderate to severe dehydration

general appearance

alert

restless, lethargic, unconscious

capillary refill

normal

prolonged or minimal

tears

present

absent

mucous membrane

moist

dry, very dry

eyes

normal

sunken; deeply sunken

breathing

present

deep; deep and rapid

quality of pulses

normal

thready; weak or impalpable

skin elasticity

instant recoil

recoil slowly; recoil > 2 s

heart rate

normal

tachycardia

urine output

normal

reduced; not passed in many hours

Evaluating dehydration with Gorelick scale [6];

4-Point Scale (Italics):

  • 4 points: Presence of 2 or more clinical signs correlating with ≥5% body weight loss from baseline.
  • 4 points: Presence of 3 or more clinical signs correlating with ≥10% body weight loss from baseline.

10-Point Scale (Based on All Signs and Symptoms):

  • ≥3 clinical signs: Associated with ≥5% body weight loss from baseline.
  • ≥7 clinical signs: Associated with ≥10% body weight loss from baseline

Some groups are at higher risk of developing complications from acute gastroenteritis. These include premature infants, very low birth weight infants, and infants below the age of 3 months. Children who are malnourished, immunosuppressed, and with chronic underlying medical conditions are also at higher risk of developing complications.

Indications for inpatient management of children presenting with acute diarrhea have been proposed, and the Table below summarizes these recommendations.

Indications for Inpatient Management of Children with Acute Diarrhoea

  • Difficulties in administrating oral rehydration therapy (patient refusal, intractable vomiting)
  • History of premature birth, chronic medical conditions, or concurrent illness, very young age
  • Parental/caregiver concern about continuing ORT at home/unable to provide adequate care
  • Persistent vomiting, high output diarrhoea, persistent dehydration
  • Uncertainty of diagnosis warranting further observation
  • Progressive symptoms or unusual irritability/drowsiness
  • Lack of easy access to hospital care if needing to return

Adapted from King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Management

Management in the Emergency Department should initially focus on correcting dehydration. Oral rehydration solution (ORS) is recommended for all children with mild to moderate dehydration.

To calculate the volume of oral replacement therapy (ORT), the first step is to estimate the degree of dehydration based on history and physical examination findings (see Table below). The desired volume of ORS is then calculated based on the degree of dehydration (30 to 50 mL/kg for mild and 60 to 80 mL/kg for moderate dehydration). 25% of the calculated volume of ORS is given every hour for the first four hours and ongoing losses can be replaced at 10 mL/kg for each stool and 2 mL/kg for each emesis. The patient needs reassessment at the end of the first few hours and those with no clinical deterioration may have a 2 to 4-hour trial with ORT. If the child is unable to keep up with ongoing losses and if volume replacement is not adequate at the end of 8 hours, IV rehydration is recommended. Ondansetron is a selective 5-hydroxytryptamine type 3 receptor antagonist, a useful adjunct in treating AGE. It acts on peripheral and central chemoreceptors to alleviate nausea. It has been shown to decrease vomiting, improve oral intake, and reduce the need for intravenous fluid resuscitation and hospital admissions [7].

Assessment of Degree of Dehydration

Mild dehydration (3%-5%)

Moderate dehydration (5%-10%)

Severe dehydration (> 10%)

Mental status

Alert

Irritable

Lethargy

Heart rate

Normal

Increased

Increased

Quality of pulses

Normal

Normal to decreased

Decreased to thready

Mucous membranes

Wet

Slightly dry

Dry

Capillary refill

< 2 seconds

> 2 seconds

> 2 seconds

Blood pressure

Normal

Normal

Normal to decreased

Respirations

Normal

Tacypnea

Tachypnea, deep

Fontanelle

Normal

Sunken

Sunken

Eyes

Normal

Slightly sunken, decreased tears

Sunken, cries without tears

Urine output

Normal to decreased

Decreased

Oliguric or anuric

Skin turgor

Normal

Slightly reduced

Reduced

Children with severe dehydration, signs of shock, failed attempts with oral rehydration therapy, intractable vomiting, hypoglycemia, or electrolyte derangements require intravenous fluid resuscitation, which is often initiated as a 20 mL/kg bolus of 0.9% of sodium chloride in ED. These patients need frequent re-evaluation to review their response to IV hydration. Improvements in mental status, tachycardia, capillary refill time, and urine production are some signs that signal a good response to intravenous resuscitation. After initial resuscitation, patients will need an evaluation of their maintenance fluid needs, which could be either intravenous fluid therapy or ORT, depending on the patient’s clinical status. Maintenance fluids are calculated based on the child’s weight using the 4-2-1 Holliday-Segar Rule.

Holliday-Segar Rule for Maintenance Fluid Calculation

Body Weight

mL/kg/hr

mL/kg/day

First 10 kg

4

100

Second 10 kg

2

50

Each additional kg

1

20

Children who require multiple fluid boluses without signs of improvement should be investigated for other serious conditions such as adrenal insufficiency, cardiogenic or septic shock, etc. It is important to note that rapid correction of serum sodium levels can lead to osmotic demyelination syndrome in hyponatremia and cerebral edema in hypernatremia.

In children with hypoglycemia, glucose can be replaced as per the “rule of 50,” where the percent dextrose multiplied by the number of mL per kilogram equals 50. Neonates often get 10% dextrose solution at 5mL/kg, children between 1 month to 8 years of age (or 25 kg weight) can be given 2mL/kg of 25% dextrose. 50% of dextrose at 1mL/kg can be used safely in older children. The higher tonicity of 25% and 50% dextrose solutions poses a risk of tissue necrosis if extravasation occurs during peripheral IV infusion.
 
Antibiotics are not indicated in viral gastroenteritis and most cases of uncomplicated bacterial gastroenteritis. Considerations can be made for very young infants, immunocompromised, and those with chronic underlying medical conditions. The WHO recommends zinc supplementation for children under 5 years suffering from AGE in developing countries [8]. Studies showing the efficacy of probiotics are inconclusive and further research is needed to establish the safety and efficacy of probiotics in children with AGE [9].

When To Admit This Patient

Most cases of AGE are self-limiting and can be managed on an outpatient basis after a brief period of observation in the ED. Parents and caregivers should be given appropriate discharge instructions emphasizing hygiene and hand-washing techniques to prevent the further spread of the illness. Breastfeeding/routine diet should be continued at home, and supplemental electrolyte solutions may be recommended. Parents and caregivers should be educated to recognize the signs of dehydration and advised to bring the child back to the ED for these. Children with intractable vomiting, severe dehydration, failure to maintain oral hydration, electrolyte derangements, deteriorating clinical status, and those at high risk for complications (very low birth weight infants, < 3 months old, immunosuppressed, and children with chronic medical problems) should be admitted to hospital.

Revisiting Your Patient

History-taking reveals that Zoey has not had much to drink or eat in the past 12 hours, and there has been an outbreak of gastroenteritis in the nursery that she attends. There has been no blood in the stools, and Mum says that Zoey has been very sleepy for the last few hours. Her vaccinations are up to date, and she has no other medical history of note.

On examination, she is irritable when you approach her, and your systematic examination reveals the following:
CNS – Irritable, no signs of meningism, anterior fontanelle closed
HEENT – Dry mucous membranes, slightly sunken eyeballs
Respiratory – Mild tachypnea, bilateral air entry with clear breath sounds
CVS – Central capillary refill 3 seconds, tachycardia, BP 88/50
Abdomen – Soft, lax and non-tender. Bowel sounds ++, no mass palpable
Skin – Slightly reduced skin turgor, no rash

Next steps?

Your examination reveals no red flags of meningitis/sepsis or surgical abdomen. Given the recent outbreak of gastroenteritis in her nursery, you make a provisional diagnosis of acute gastroenteritis for Zoey. Your clinical assessment estimates the degree of dehydration to be moderate (5-10%), and you calculate her fluid depletion to be between 600 to 800 mL (60 to 80 mL/kg). You start the patient on oral rehydration therapy aiming for at least 200 mL to be given slowly over the next hour. You guide the mother in letting the staff know if Zoey vomits or has another episode of diarrhea while in the Emergency Department.

Investigations?

You ask for a random blood sugar to rule out hypoglycemia and a urine dipstick to rule out urinary tract infection.

Review
After an hour, Zoey tolerated 250 mL of oral rehydration solution and had one episode of vomiting but no diarrhea. Her blood sugar was 4 mmol/l. She has perked up significantly and is more alert than before. Her vital signs show improvement, and you decide to give her Ondansetron and continue the ORT.

After two hours, Zoey has tolerated around 400 mL of ORS and is more alert and interactive now. Her vitals are normal, and she has not had any further episodes of diarrhea or vomiting. She has also passed some urine, which has been tested and found to be negative for infection.

Mum was advised to continue oral hydration at home as well as the slow introduction of a regular diet and to come back to ED if Zoey could not tolerate orally, had intractable vomiting, any blood in her stools, high-grade fever, or change from her baseline mental status. Zoey was discharged from the ED and would follow up with her primary physician in the community.

Authors

Picture of Neha Hudlikar

Neha Hudlikar

Emergency Department, Zayed Military Hospital, Abu Dhabi

Picture of Abdulla Alhmoudi

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

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References

  1. McDermott KW, Stocks C, Freeman WJ. Overview of Pediatric Emergency Department Visits, 2015. In: Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. Rockville (MD): Agency for Healthcare Research and Quality (US); August 7, 2018.
  2. Hartman RM, Cohen AL, Antoni S, et al. Risk Factors for Mortality Among Children Younger Than Age 5 Years With Severe Diarrhea in Low- and Middle-income Countries: Findings From the World Health Organization-coordinated Global Rotavirus and Pediatric Diarrhea Surveillance Networks [published correction appears in Clin Infect Dis. 2023 Jan 6;76(1):183]. Clin Infect Dis. 2023;76(3):e1047-e1053. doi:10.1093/cid/ciac561
  3. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated?. JAMA. 2004;291(22):2746-2754. doi:10.1001/jama.291.22.2746
  4. Falszewska A, Szajewska H, Dziechciarz P. Diagnostic accuracy of three clinical dehydration scales: a systematic review. Arch Dis Child. 2018;103(4):383-388. doi:10.1136/archdischild-2017-313762
  5. Freedman SB, Vandermeer B, Milne A, Hartling L; Pediatric Emergency Research Canada Gastroenteritis Study Group.
  6. Pringle K, Shah SP, Umulisa I, et al. Comparing the accuracy of the three popular clinical dehydration scales in children with diarrhea. Int J Emerg Med. 2011;4:58. Published 2011 Sep 9. doi:10.1186/1865-1380-4-58
  7. Tomasik E, Ziółkowska E, Kołodziej M, Szajewska H. Systematic review with meta-analysis: ondansetron for vomiting in children with acute gastroenteritis. Aliment Pharmacol Ther. 2016;44(5):438-446. doi:10.1111/apt.13728Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis. J Pediatr. 2015;166(4):908-16.e166. doi:10.1016/j.jpeds.2014.12.029
  8. Goldman RD. Zinc supplementation for acute gastroenteritis. Can Fam Physician. 2013;59(4):363-364.
  9. Cameron D, Hock QS, Kadim M, et al. Probiotics for gastrointestinal disorders: Proposed recommendations for children of the Asia-Pacific region. World J Gastroenterol. 2017;23(45):7952-7964. doi:10.3748/wjg.v23.i45.7952

Additional Resources

King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

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.

More dehydration content on iem-student.org

Question Of The Day #50

question of the day
~ Joseph Ciano, USA ~ Leave a comment

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

  • A) IV Physostigmine
  • B) IV Potassium iodide
  • C) IV Propranolol
  • D) PO Propylthiouracil (PTU)

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient arrives hyperthermic, tachycardic in atrial fibrillation, diaphoretic, and altered with psychotic behavior.  Thyroid storm, the most severe manifestation of hyperthyroidism, should always be on the differential diagnosis in patients with fever and altered mental status.  Other considerations are sepsis, sympathomimetic overdose, anticholinergic overdose, serotonin syndrome, and pheochromocytoma. 

This patient has thyroid storm, a life-threatening endocrine emergency that requires prompt recognition and treatment.  Symptoms of thyroid storm include altered mental status, psychosis, seizures, coma, tachycardia, atrial fibrillation, high-output heart failure, dyspnea, vomiting, diarrhea, weight loss, and anterior neck enlargement.  Severe hyperthyroidism should have a low-undetectable TSH level with elevated T3/T4 levels, but in acute illness these levels may be unreliable.  For this reason, the diagnosis and treatment of thyroid storm should be based on clinical grounds.

An anticholinergic toxidrome can appear similar to this patient with tachycardia, hypertension, agitation, and altered mental status.  A key differentiating factor is diaphoresis.  Patients with anticholinergic ingestions should have dry skin, not wet skin. The treatment for anticholinergic toxicity is benzodiazepines and IV physostigmine (Choice A) if symptoms are unresponsive to benzodiazepines.  Physostigmine is not the best next step in this scenario. 

Treatment of thyroid storm is algorithmic.  First, beta blockade (Choice C) should be given to control the heart rate and block T4 to T3 conversion, next anti-thyroid medications (Methimazole or Propylthiouracil (Choice D)) should be given to block thyroid hormone synthesis, and lastly corticosteroids and inorganic iodine (Choice B) can be given to block release of stored thyroid hormone.  The best next step in managing this patient with thyroid storm is administration of IV Propranolol (Choice C).  Propranolol helps manage the tachycardia, systemic symptoms, and also inhibits conversion of T4 to T3. 

 Correct Answer: C

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References

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Physiologically Difficult Airway – Metabolic Acidosis

Physiologically Difficult Airway - Metabolic Acidosis
~ Jule Santos, Brasil ~ Leave a comment

Case Presentation

A 32-year-old male with insulin-dependent diabetes mellitus came to your emergency department for shortness of breath. He was referred to the suspected COVID-19 area. His vitals were as follows: Blood pressure, 100/55 mmHg; pulse rate, 135 bpm; respiratory rate, 40/min; saturation on 10 liters of oxygen per minute, 91%; body temperature, 36.7 C. His finger-prick glucose was 350 mg/dl.

The patient reported that he had started to feel ill and had an episode of diarrhea 1 week ago. He developed a dry cough and fever in time. He started to feel shortness of breath for 2 days. He sought out the ER today because of the difficulty breathing and abdominal pain.

The patient seemed alert but mildly agitated. He was breathing effortfully and sweating excessively. On physical examination of the lungs, you noticed fine crackles on the right. Despite the patient reported abdominal pain, there were no signs of peritonitis on palpation.

An arterial blood gas analysis showed: pH 7.0, PCO2: 24, pO2: 56 HCO3: 8 Lactate: 3.

The point-of-care ultrasound of the lungs showed B lines and small foci of subpleural consolidations on the right.
At this point, what are your diagnostic hypotheses?

Two main diagnostic hypotheses here are:

  • Diabetic ketoacidosis (Hyperglycemia + metabolic acidosis)
  • SARS-CoV2 pneumonia

We avoid intubating patients with pure metabolic decompensation of DKA if possible, as they respond to hydration + insulin therapy + electrolyte replacement well and quickly. 

But in this scenario, the patient is extremely sick and has complicating medical issues, such as an acute lung disease decompensating the diabetic condition, probably COVID19. Considering these extra issues may complicate the recovery time and increase the risk of respiratory failure, you decide to intubate the patient in addition to the treatment of DKA.

You order lab tests and cultures. You start hydration and empirical antibiotics while starting preoxygenation and preparing for intubation.

Will this be a Difficult Airway?

Evaluating the patient for the predictors of a difficult airway is a part of the preparation for intubation. Based on your evaluation, you should create an intubation plan. 

This assessment is usually focused on anatomical changes that would make it difficult to manage the airway (visualization of the vocal cords, tube passage, ventilation, surgical airway), thereby placing the patient at risk.

“Does this patient have any changes that will hinder opening the mouth, mobilizing the cervical region, or cause any obstruction for laryngoscopy? Does this patient have any changes that hinder the use of Balloon-Valve-Mask properly, such as a large beard? What about the use of the supraglottic device? Does this patient have an anatomical alteration that would hinder emergency cricothyroidotomy or make it impossible, like a radiation scar? ”

So the anatomically difficult airway is when the patient is at risk if you are unable to intubate him due to anatomical problems.

The physiologically difficult airway, however, is when the patient has physiological changes that put him at risk of a bad outcome during or shortly after intubation. Despite intubation. Or because of intubation, because of its physiological changes due to positive pressure ventilation.

These changes need to be identified early and must be mitigated. You need to recognize the risks and stabilize the patient before proceeding to intubation or be prepared to deal with the potential complications immediately if they happen.

5 main physiological changes need attention before intubation are: hypoxemia, hypotension, severe metabolic acidosis, right ventricular failure, severe bronchospasm.

Back to our patient: Does he have physiologically difficult airway predictors?

  • SI (Shock Index): 1.35 (Normal <0.8) – signs of shock
  • P / F: 93 (Normal> 300) – Severe hypoxemia
  • pH: 7.0: Severe metabolic acidosis – expected pCO2: 20 (not compensating)
  • qSOFA: 2 + Lactate: 3 (severity predictor)

Physiologically Difficult Airway

"Severely critical patients with severe physiological changes who are at increased risk for cardiopulmonary collapse during or immediately after intubation."

Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused.

Severe Metabolic Acidosis

In this post, we will focus only on the compensation of the metabolic part, but do not forget that this is a patient who needs attention on oxygenation and hemodynamics as well. That is, this is intubation with very difficult predictions.

What happens during the rapid sequence of intubation in severe metabolic acidosis?

To perform the procedure, the patient needs to be in apnea. During an apnea, pulmonary ventilation is decreased and the CO2 is not “washed” from the airway. These generate an accumulation of CO2, an acid, decreasing blood pH. In a patient with normal or slightly altered pH, this can be very well-tolerated, but in a patient with a pH of 7.0, an abrupt drop in this value can be ominous.

We know that the respiratory system is one of the most important compensation mechanisms for metabolic acidosis and it starts its action in seconds, increasing the pH by 50 to 75% in 2 to 3 minutes, guaranteeing the organism time to recover. So, even seconds without your proper actions can be risky for critical patients.

In addition, it must be remembered that increased RF is the very defense for the compensation of metabolic acidosis, and most of the time the organism does this very well. So if after the intubation the NORMAL FR and NORMAL minute volume are placed in the mechanical ventilator parameters, again there is an increase in CO2 and a further decrease in pH.

And what’s wrong? After all, a little bit of acidosis even facilitates the release of oxygen in the tissues because it deflects the oxyhemoglobin curve to the right, right?

Severe metabolic acidosis (pH <7.1) can have serious deleterious effects:

  • Arterial vasodilation (worsening shock)
  • Decreased myocardial contractility
  • Risks of arrhythmias
  • Resistance to the action of DVAs
  • Cellular dysfunction

What to do?

Always the primary initial treatment is: treating the underlying cause! In patients with severe metabolic acidosis, it is best to avoid intubation! Especially in metabolic ketoacidosis, which as hydration and insulin intake improves, there is a progressive improvement in blood pH.

Sodium bicarbonate

The use of sodium bicarbonate to treat metabolic acidosis is controversial, especially in non-critical acidosis values ​​(pH> 7.2). If you have acute renal failure associated, its use may be beneficial by postponing the need for renal replacement therapy (pH <7.2).

As for DKA, where sodium bicarbonate is used to the ketoacidosis formed by erratic metabolism due to the lack of insulin and no real deficiency is present, its use becomes limited to situations with pH <6.9.

The dose is empirical, and dilution requires a lot of attention (avoid performing HCO3 without diluting!)

NaHCO3 100mEq + AD 400ml

Run EV in 2h

If K <5.3: Associate KCl 10% 2amp

I would make this solution and leave it running while proceeding with the intubation preparations.

Attention: Remember, according to the formula below, that HCO3 is converted to CO2, and if done in excess, is associated with progressive improvement of the ketoacidosis and recovery of HCO3 from the buffering molecules. In a patient already with limited ventilation, its increase can cause deviation of the curve for the CO2 increase, which is also easily diffused to the cells and paradoxically decrease the intracellular pH, in addition to carrying K into the cell.

H + + HCO3 – = H2CO3 = CO2 + H2O

Mechanical ventilation

I think the most important part of the management of these patients is the respiratory part.

If you choose the Rapid Sequence Intubation: Prepare for the intubation to be performed as quickly as possible: Use your best material, choose the most experienced intubator, put the patient in ideal positioning, decide and apply medications skillfully, to ensure the shortest time possible apnea.

You will need personnel experienced in Mechanical Ventilation and you must remember to leave the ventilatory parameters adjusted to what the patient needs and not to what would be normal!

I found this practice very interesting: First, you calculate what the expected pCO2 should be for the patient, according to HCO3:

Winter’s Equation (Goal C02) = 1.5 X HCO3 + 8 (+/- 2)

And then, according to this table, you try to reach the VM Volume Minute value.
Goal CO2 Minute Ventilation
40 mmHg
6-8 L
30 mmHg
12-14 L
20 mmHg
18-20 L

These are just initial parameters. With each new blood gas analysis repeated in 30 minutes to an hour, you re-make fine adjustments using the formula below:

Minute volume = [PaCO2 x Minute volume (from VM)] / CO2 Desired

With the treatment of ketoacidosis, new parameters should be adjusted, hopefully for the better.

Another safer option for these patients would be to use the Awake Patient Intubation technique so that you would avoid the apnea period. However, Awake Patient Intubation Technique is contraindicated in suspected or confirmed COVID-19 cases due to the risk of contamination.

That’s it, folks, send your feedback, your experiences, and if you have other sources!

Further Reading

  1. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 3: Severe Metabolic Acidosis”, REBEL EM blog, June 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-3-severe-metabolic-acidosis/.
  2. Justin Morgenstern, “Emergency Airway Management Part 2: Is the patient ready for intubation?”, First10EM blog, November 6, 2017. Available at: https://first10em.com/airway-is-the-patient-ready/.
  3. Salim Rezaie, “How to Intubate the Critically Ill Like a Boss”, REBEL EM blog, May 3, 2019. Available at: https://rebelem.com/how-to-intubate-the-critically-ill-like-a-boss/.
  4. Salim Rezaie, “RSI, Predictors of Cardiac Arrest Post-Intubation, and Critically Ill Adults”, REBEL EM blog, May 10, 2018. Available at: https://rebelem.com/rsi-predictors-of-cardiac-arrest-post-intubation-and-critically-ill-adults/.
  5. Salim Rezaie, “Critical Care Updates: Resuscitation Sequence Intubation – pH Kills (Part 3 of 3)”, REBEL EM blog, October 3, 2016. Available at: https://rebelem.com/critical-care-updates-resuscitation-sequence-intubation-ph-kills-part-3-of-3/.
  6. Lauren Lacroix, “APPROACH TO THE PHYSIOLOGICALLY DIFFICULT AIRWAY”, https://emottawablog.com/2017/09/approach-to-the-physiologically-difficult-airway/
  7. Scott Weingart. The HOP Mnemonic and AirwayWorld.com Next Week. EMCrit Blog. Published on June 21, 2012. Accessed on July 15th 2020. Available at [https://emcrit.org/emcrit/hop-mnemonic/ ].
  8. IG: @pocusjedi: “Pocus e Coronavirus: o que sabemos até agora?”https://www.instagram.com/p/B-NxhrqFPI1/?igshid=14gs224a4pbff

References

  1. Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused. Br J Anaesth. 2020;125(1):e18-e21. doi:10.1016/j.bja.2020.04.008
  2. Mosier JM, Joshi R, Hypes C, Pacheco G, Valenzuela T, Sakles JC. The Physiologically Difficult Airway. West J Emerg Med. 2015;16(7):1109-1117. doi:10.5811/westjem.2015.8.27467
  3. Irl B Hirsch, MDMichael Emmett, MD. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on July 15, 2020.)
  4. Cabrera JL, Auerbach JS, Merelman AH, Levitan RM. The High-Risk Airway. Emerg Med Clin North Am. 2020;38(2):401-417. doi:10.1016/j.emc.2020.01.008
  5. Guyton AC, HALL JE. Tratado de fisiologia medica. 13a ed. Rio de Janeiro(RJ): Elsevier, 2017. 1176 p.
  6. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010;6(5):274-285. doi:10.1038/nrneph.2010.33
  7. Calvin A. Brown III, John C. Sakles, Nathan W. Mick. Manual de Walls para o Manejo da Via Aérea na Emergência. 5. ed. – Porto Alegre: Artmed, 2019.
  8. Smith MJ, Hayward SA, Innes SM, Miller ASC. Point-of-care lung ultrasound in patients with COVID-19 – a narrative review [published online ahead of print, 2020 Apr 10]. Anaesthesia. 2020;10.1111/anae.15082. doi:10.1111/anae.15082
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Hypoglycemia – A Rural Perspective

hypoglycemia - a rural perspective
~ Carmina Shrestha, Nepal ~ Leave a comment

Waiting for patients is among some of the weird perks of working in a rural ER. “Too little isn’t fun as well”, said an enthusiastic new paramedic at Beltar PHC. Later that night, I’d find a funny connection between what he said and what followed.

A 56Y/M patient is brought to the ER on a particularly silent evening. Following the usual ER premise; I reach the department from upstairs. The patient was unconscious when I arrived. A paramedic was trying to open a peripheral line, and a nurse was taking a pulse oximeter reading while keeping the patient at 2L via nasal cannula. The bystanders who brought him had no clue of what had happened or if the patient had any comorbidity. As I grabbed the glucometer from the drawer, I could not help but remember how in med school exams all the hypoglycemic patients were medics who injected themselves with insulin. As I poked the patient with a lancet and measured his blood glucose, I realized the paramedic had already given up trying to get IV access. “I couldn’t get in”, he said. The glucometer beeped exactly then as if to confirm “this is trouble” – 37! “That is hypoglycemia”, I exclaimed!

Although there is no universally accepted definition of hypoglycemia (low blood glucose), a level below 60 rings the bell. As I tried to establish the line, I requested my nurse to prepare a thick paste of glucose powder. Of all the medicine I was taught, one thing I’ve found the most useful is the “available” medicine. Sure, start with a bolus of the glucose-containing solution: D50 or D10, if you cannot get IV access go for IM glucagon and so forth. But when you’re working in a setting where you second guess yourself for wasting a lancet while checking a patient’s blood glucose, IM glucagon becomes nothing more than a very good test question.

I could not get the line started either. Minutes after we applied the glucose paste on the buccal mucosa, the patient woke up. The sigh of relief was audible in the small ER of our PHC. Eventually, we were able to feed the patient per oral. The patient turned out to be diabetic who thought, “insulin is a medicine, hence should not be ignored, but the food is optional.”

Clinical hypoglycemia is sometimes defined as blood glucose low enough to cause symptoms. For most people, this occurs at 50-60 mg/dL. Clinically significant hypoglycemia is confirmed by the presence of the ‘Whipple triad’. Yap, that’s the same Allen Whipple, the American surgeon who also coined the Whipple procedure! The presence of symptoms consistent with hypoglycemia, a low serum glucose level, and resolution of the symptoms and signs of hypoglycemia with the administration of glucose is what confirms hypoglycemia.

Because diabetics are most prone to get hypoglycemic, in a diabetic patient, hypoglycemia is defined as a self-monitored blood glucose level ≤ 70mg/dL. Everyone else must have a documented experience of Whipple’s triad for the diagnosis. There is also something called relative hypoglycemia, it occurs when a patient with diabetes reports hypoglycemic symptoms, but the blood glucose remains above 70 mg/dL. This still requires treatment. Remember, we treat patients, not numbers.

The causes of hypoglycemia can be diverse, but the horses include missed meals or overnight fasting but still using hypoglycemic agents (sulphonylureas, insulin) in a person with diabetes. Be vigilant about recent exercise enthusiasts, alcohol ingestion, weight loss, and renal failure (which can reduce insulin clearance).

Signs and symptoms of hypoglycemia in non-diabetic patients are generally fairly obvious. Sympathetic autonomic nervous system activation symptoms like nervousness, anxiety, tremulousness, sweating, palpitations, shaking, dizziness, hunger, and symptoms due to decreased availability of glucose to the brain; confusion, weakness, drowsiness, speech difficulty, incoordination, odd behavior are seen below the commonly quoted glycemic values of 50-60. In severe cases, hypoglycemia may result in seizures, coma, or death.

A logical treatment flowchart should start with a glucose-containing solution: D50 or D10. In regards to D50, be aware that the bolus may cause rebound hypoglycemia, may overshoot glycemic targets and is hypertonic hence should be given slowly over 2-5 minutes. There has been extensive debate over D50 vs D10, here is what I try to keep in mind; If using D50, give 1 amp at a time over 2-5 mins. If D10, a 100ml bolus over 2 mins. Check the patients’ glucose levels often.

Remember both of those approaches require you to have IV access. Intramuscular glucagon (5mg) may be given to raise serum glucose levels. Keep in mind two things: the efficacy of glucagon is dependent upon hepatic glycogen stores. Patients with prolonged hypoglycemia may have a minimal response and repeating glucagon does not make much sense.

If the blood glucose goes back to > 60mg/dL in a non-diabetic patient, and >70mg/dL in a diabetic patient and/or there is an improvement in symptoms, patients who can eat should do so otherwise IV dextrose drip (D5W at 75-100 mL/hr) is the way to go.

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Hypokalemic Periodic Paralysis in the ED

Hypokalemic Periodic Paralysis in the ED
~ Sumaiya Hafiz, UAE ~ 1 Comment

Case Presentation

A middle-aged man with a two days history of weakness in his legs. The patient works as a construction worker and is used to conducting heavy physical activity.

After a thorough history and examination, the weakness was reported in the lower extremities with a power of 2/5, whereas the power in upper extremities was 4.5/5, Achilles tendon reflex was reduced, plantar response and other reflexes were intact, with normal sensation. Rest of the examination is unremarkable.

The vitals are within normal ranges, Blood investigations include – Urea and electrolytes, liver and renal function, full blood count, thyroid function tests, creatine kinase, urine myoglobin, vitamin B12 and folic acid levels.

Potassium level was 1.7 mEq/L (normal 3.5-5.5), and all other parameters were within normal ranges.

The ECG showed inverted T waves and the presence of U waves. An Example of an ECG:

ECG-hypokalemia

Hypokalaemia

Hypokalemic periodic paralysis is a rare disorder that may be hereditary as the primary cause, or secondary due to thyroid disease, strenuous physical activity, a carbohydrate-rich meal and toxins. The patients are mostly of Asian origin.

The most common presentation is of symmetrical weakness in lower limbs, with a low potassium level and ECG changes of hypokalemia. The patients may have a history of similar weaknesses which may be several years old. An attack may be triggered by infections, stress, exercise and other stress-related factors.

The word ‘weakness’, can lead to physicians thinking about stroke, neurological deficits and other life-threatening illnesses such as spinal cord injuries associated with high morbidity and mortality which need to be ruled out in the ED.

In this case, history and examination are vital. Weakness in other parts of the body, a thorough neurological examination are important aspects.

Patients are monitored and treated with potassium supplements (oral/Intravenous) until the levels normalize. ECG monitoring is essential, as cardiac function may be affected. 

The patient should be examined to assess the strength and should be referred for further evaluation and to confirm the diagnosis.

The differential diagnosis for weakness in lower limb include :

  1. Spinal cord disease (https://iem-student.org/spine-injuries/)
  2. Guillain barre syndrome
  3. Toxic myositis
  4. Trauma
  5. Neuropathy
  6. Spinal cord tumour

References

[cite]