Upper GI Bleeds Core Concepts

Join the EMGuideWire team as they tackle the tough core concepts of how to manage the patients with simple and critical Upper Gastrointestinal Bleeds. Know what medicines are imperative to start and what ones may be discussed with your consultants.

EM@3AM: Hypernatremia

Author: Mark M. Ramzy, DO, EMT-P (@MarkRamzyDO, EM Resident Physician, Drexel University, Department of Emergency Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 61-year-old male presents in middle of July with altered mental status. He is accompanied by his son who states the patient has been increasingly weak for the past three days. The patient has been having multiple episodes of non-bloody diarrhea with associated decreased appetite. Further history reveals the son has yet to install an air-conditioning unit in the patient’s room at home. The patient is unable to provide any additional information or review of systems due to his confusion.

Initial triage vital signs include BP 104/66, HR 111, RR 18, SpO99%, Temp 36.9 oC.

Exam findings include an awake elderly Caucasian male not oriented to person, place, time, or event. He appears clinically dehydrated with dry mucous membranes and poor skin turgor with tenting. Remaining exam shows no pertinent positives. An initial rapid VBG reveals a sodium of 161 mEq/L.

What is the diagnosis, and what investigations, therapies, and complications do you need to consider?


Answer: Hypernatremia 

Definition: Serum or plasma sodium [Na+] greater than 145 mEq/L and serum osmolality greater than 295 mOsm/L.

  • Severe hypernatremia occurs at [Na+] greater than 160 mEq/L, or if symptoms due to hypernatremia are present.
  • The condition is mainly a result of a deficit in total body water (TBW) or a net gain of Na+­­. This is most commonly due to deficit in TBW.

Causes and risk factors: Limited availability to free water, kidneys failure to concentrate urine, increased salt intake, or any clinical situation that interferes with a patient’s ability to sense thirst. The loss of free water in diarrhea or excessive urination may also cause significant hypernatremia.1,2  Nephrogenic or central diabetes insipidus may be a cause of hypernatremia.

  • Infants, recently hospitalized patients, and the elderly are at higher risk of developing hypernatremia.1,2
  • Of note, hypernatremia not only increases mortality but when present in elderly patients, it is a marker for severe systemic illness.3,4
  • In both elderly and hospitalized patients, hypernatremia is often iatrogenic and can result from the inappropriate administration of intravenous fluids (IVF).4,5

History: Symptoms often include thirst, nausea, vomiting, fatigue, weakness, lethargy, muscle twitching, spasms, seizures, altered mental status, and coma. Take note of environmental factors that may be contributing to increased water loss. Ask about medications, illnesses, co-morbidities, intake, and output.

Physical Exam: Exam findings vary but often include hypotension, tachycardia, sunken eyes, dry mucous membranes, poor skin turgor, and in severe cases, altered mental status. Depending on the severity and time without intervention, coma, seizures, and shock may occur.

Management: Regardless of the initial sodium level, correcting the sodium either too quickly or too slowly is associated with an increased risk of death.6  Therefore the treatment of hypernatremia requires appropriate timing and a systematic approach.

  1. Resuscitate: Volume deficits and hypoperfusion must be quickly corrected if they are present. To do so, use of isotonic saline solution is recommended. Again, this is only if the patient has evidence of hypoperfusion noted by persistent hypotension or end-organ damage (ie. elevated lactate, AKI, etc). It may seem counterproductive giving a fluid with sodium to a hypernatremic patient, however, the goal is to restore homeostatic mechanisms of sodium balance. The rate of correction is extremely vital to remember: do not lower more than 0.5 mEq/L/h or 10 to 12 mEq over 24 hours. If the patient is not hypovolemic and perfusing well, then use of hypotonic fluids such as D5W or ¼ normal saline is appropriate.
  2. Investigate: Identify the underlying cause of the hypernatremia and address it. Look for sources of infection if the patient has a fever, as this form of extrarenal water loss may contribute to hypernatremia. Obtaining a urine sodium and urine osmolality will help identify the cause of low volume status and better direct management. Recognizing other electrolyte abnormalities such as hypokalemia and hypercalcemia may point towards renal causes of hypernatremia. A new diagnosis of sarcoidosis, multiple myeloma, or a pituitary tumor may raise suspicion for hypernatremia secondary to nephrogenic or central diabetes insipidus. Start with ordering a Basic Metabolic Profile (BMP), extended electrolytes (ie. magnesium, phosphorus, etc), urine sodium, and urine osmolality (or urine specific gravity if urine osmolality is not readily available).
  3. Rehydrate: Understanding the effect of 1 liter of any infusate is vital to the management of the hypernatremic patient and correction of the sodium. Knowing how much sodium is in each of the infusates used can more accurately correct the sodium and also help you track if treatment is heading in the right direction (See Table 1). Scott Weingart recommends the use of Adrogue Madias’ formula to see how much the infusate administered affects the patient’s sodium with rechecks every couple of hours.7

Complications: Hypernatremia when untreated can result in several complication such as altered mental status, rhabdomyolysis, seizures, and impaired glucose use.

Pearls:

  1. ResuscitateCorrect volume deficits and hypoperfusion. Do not lower more than 0.5 mEq/L/h or 10 to 12 mEq over 24 hours. If the patient is not hypovolemic, use D5W.
  2. InvestigateAddress the underlying cause of hypernatremia. Consider electrolyte imbalances, sarcoidosis, nephrogenic or central diabetes insipidus.
  3. RehydrateUse Adrogue Madias’ formula to understand how much each infusate affects the patient’s sodium and adjust treatment course with frequent checks.

A 32-year-old man who became lost while hiking in the desert is rescued after several days. He is lethargic, confused, and appears severely dehydrated. His weight is 75 kg and his serum sodium level is 158 mg/dL. What is the patient’s total body water deficit?

A. 3.8 L

B. 4.8 L

C. 5.8 L

D. 6.8 L

 

Answer: C

Hypernatremia is defined as a serum sodium concentration > 145 mEq/L. Most cases of hypernatremia are due to a total body water deficit. Heatstroke, increased insensible losses from burns or sweating, and gastrointestinal fluid losses from diarrhea or protracted vomiting can all result in hypernatremia. Patients without access to water or impaired thirst mechanisms are at particular risk for hypernatremia, including elderly bedridden patients, those with mental impairment, and patients who are in a coma. Diabetes insipidus, a condition in which there is insufficient antidiuretic hormone production, results in decreased water reabsorption and can also result in hypernatremia. Patients with hypernatremia may complain of thirst, have obvious causes of fluid losses, or may be asymptomatic. Altered sensorium is common as sodium levels rise and hypernatremia should be considered in all patients presenting with altered mental status, particularly those with severe mental impairment, head injury, or impaired access to water. The degree of hypernatremia corresponds well with the total body water deficit. A patient’s total body water can be estimated by multiplying the patient’s body weight in kilograms by 0.6. Correction factors are available for elderly patients, who have a lower muscle mass than younger individuals. Total body water (TBW) deficit in can be calculated with the following formula: TBW deficit = TBW x (serum Na+/140) – 1. In this case, the patient’s TBW deficit is (75 x 0.6) x (158/140 – 1) = (45 x (1.13 – 1) = 5.79 liters. The treatment of hypernatremia involves fluid repletion and slow correction of patient’s sodium level.

3.8 L (A), 4.8 L (B), and 6.8 L (D) are all incorrect.

 

Rosh Review Website Link


References/Further Reading:

  1. Reynolds, RM; Padfield, PL; Seckl, JR (25 March 2006). “Disorders of sodium balance”. BMJ (Clinical research ed.). 332 (7543): 702–5. doi:10.1136/bmj.332.7543.702. PMC 1410848 Freely accessible. PMID 16565125
  2. Sam R, Feizi I: Understanding hypernatremia. Am J Nephrol 36: 97, 2012.
  3. Lindner G, Funk GC, Schwarz C, et al. Hypernatremia in the critically ill is an independent risk factor for mortality. Am J Kidney Dis 2007; 50:952.
  4. Snyder NA, Feigal DW, Arieff AI. Hypernatremia in elderly patients. A heterogeneous, morbid, and iatrogenic entity. Ann Intern Med 1987; 107:309.
  5. Palevsky PM, Bhagrath R, Greenberg A. Hypernatremia in hospitalized patients. Ann Intern Med 1996; 124:197.
  6. Bataille S, Baralla C, Torro D, et al: Undercorrection of hypernatremia is frequent and associated with mortality. BMC Nephrol 2014; 15: pp. 37
  7. Scott Weingart. Podcast 187 – Hypernatremia (Uggggh!). EMCrit Blog. Published on November 28, 2016. Accessed on June 29t

The post EM@3AM: Hypernatremia appeared first on emDOCs.net - Emergency Medicine Education.

REMI 2274. Betabloqueantes en el traumatismo craneoencefálico: ¿disminuyen la mortalidad?

ARTÍCULO ORIGINAL: Beta blockers in critically ill patients with traumatic brain injury: Results from a multicenter, prospective, observational American Association for the Surgery of Trauma study. Ley EJ, Leonard SD, Barmparas G, Dhillon NK, Inaba K, Salim A, OʼBosky KR, Tatum D, Azmi H, Ball CG, Engels PT, Dunn JA, Carrick MM, Meizoso JP, Lombardo S, Cotton BA, Schroeppel TJ, Rizoli S, Chang DSJ, de León LA, Rezende-Neto J, Jacome T, Xiao J, Mallory G, Rao K, Widdel L, Godin S, Coates A, Benedict LA, Nirula R, Kaul S, Li T; Beta Blockers TBI Study Group Collaborators. J Trauma Acute Care Surg 2018; 84: 234-244. [Resumen] [Artículos relacionados]
  
INTRODUCCIÓN: La gravedad del traumatismo craneoencefálico (TCE) guarda relación con los niveles de catecolaminas en sangre, siendo mayores a mayor gravedad. La elevación es inmediata, siendo causa de inflamación y apoptosis de los tejidos cerebrales. Los betabloqueantes bloquean las catecolaminas endógenas, habiéndose encontrado que pueden disminuir la mortalidad cuando se administran precozmente [1, 2]. 
  
RESUMEN: Estudio de 25 meses prospectivo, observacional y multicéntrico realizado por el comité de The American Association for the Surgery of Trauma Multi-Institucional Trials (AAST_MIT), donde participaron 15 centros hospitalarios de Estados Unidos y Canadá para evaluar el efecto de la administración de betabloqueantes sobre la mortalidad en pacientes con TCE. Los criterios de ingreso fueron: precisar UCI, edad mayor o igual a 18 años y TCE agudo con TAC patológico. Se analizaron entre otras variables: escala de Glasgow para el coma (GCS), presión arterial al ingreso, TAC craneal, tratamiento previo con betabloqueantes, anticoagulantes o antiagregantes, Injury Severity Score (ISS), mortalidad, escala pronóstica de Glasgow (GOS) y días de estancia hospitalaria. El uso de betabloqueantes quedó a discreción del médico según arritmias, HTA, etc. Se registraron todos los tipos de betabloqueantes utilizados, y se analizó el subgrupo particular de los que recibieron propanolol [3]. Hubo un total de 2.252 pacientes con TCE. Los pacientes que recibieron betabloqueantes (n=1.120, 49,7%) tenían mayor edad, mayor probabilidad de estar tratados con anticoagulantes o tomar betabloqueantes previamente al traumatismo, mayor porcentaje de intubación y mayor gravedad del TCE (puntuación head-AIS). La mortalidad global a los 30 días fue 15,8% y fue menor de forma significativa en los pacientes que recibieron betabloqueantes (13,8% frente a 17,7%, P = 0,013). En el 31,6% fueron dados en el día 1º de ingreso hospitalario y el 82,7% al día 5º. El subgrupo que recibieron propanolol (n=354) respecto a otros betabloqueantes (n=766) fueron más jóvenes, tenían más probabilidad de hipotensión e intubación al ingreso, menor GSC, mayor ISS y head AIS. La mortalidad fue significativamente menor en pacientes tratados con propanolol respecto al resto de betabloqueantes.
   
COMENTARIO: El estudio es importante al ser el primer estudio multicéntrico en encontrar una disminución de la mortalidad con el uso de betabloqueantes en el TCE. El mecanismo exacto no es conocido; sin embargo, en modelos experimentales los betabloqueantes incrementan la perfusión cerebral, disminuyen la hipoxia y mejoran el metabolismo de la glucosa. El estudio muestra además superioridad del propanolol respecto al resto de betabloqueantes en disminuir la mortalidad en el TCE. Sin embargo, son necesarios ensayos clínicos que superen las limitaciones de los estudios observacionales [4, 5].
   
Encarnación Molina Domínguez
Hospital General Universitario de Ciudad Real.
© REMI, http://medicina-intensiva.com. Julio 2018.
      
ENLACES:
  1. The Effect of β-blockade on Survival After Isolated Severe Traumatic Brain Injury. Mohseni S, Talving P, Thelin EP, Wallin G, Ljungqvist O, Riddez L. World J Surg. 2015 Aug;39(8):2076-83. [PubMed]
  2. Early propranolol after traumatic brain injury is associated with lower mortality. Ko A, Harada MY, Barmparas G, Thomsen GM, Alban RF, Bloom MB, Chung R, Melo N, Margulies DR, Ley EJ. J Trauma Acute Care Surg. 2016 Apr;80(4):637-42. [PubMed]
  3. Traumatic brain injury and β-blockers: not all drugs are created equal. Schroeppel TJ, Sharpe JP, Magnotti LJ, Weinberg JA, Clement LP, Croce MA, Fabian TC. J Trauma Acute Care Surg. 2014 Feb;76(2):504-9; discussion 509. [PubMed]
  4. Beta-blockers and Traumatic Brain Injury: A Systematic Review, Meta-analysis, and Eastern Association for the Surgery of Trauma Guideline. Alali AS, Mukherjee K, McCredie VA, Golan E, Shah PS, Bardes JM, Hamblin SE, Haut ER, Jackson JC, Khwaja K, Patel NJ, Raj SR, Wilson LD, Nathens AB, Patel MB. Ann Surg. 2017 Dec;266(6):952-961. [PubMed]
  5. Therapeutic effect of beta-blocker in patients with traumatic brain injury: A systematic review and meta-analysis. Chen Z, Tang L, Xu X, Wei X, Wen L, Xie Q. J Crit Care. 2017 Oct;41:240-246. [PubMed]
BÚSQUEDA EN PUBMED:
  • Enunciado: Efecto de los betabloqueantes sobre la mortalidad en el TCE
  • Sintaxis: Beta-blockers head injury mortality
  • [Resultados]