Should I treat asymptomatic blood pressure (BP) elevation in my hospitalized patient with well-controlled BP prior to admission?

In contrast to the management of acute symptomatic hypertension in the hospital, evidence-based guidelines on when to treat asymptomatic BP elevation (eg, >160/90 mm Hg without signs of end-organ injury) in patients without acute conditions (eg, acute myocardial infarction [MI] or acute ischemic stroke) are lacking. The literature suggests, however, that a more permissive approach is appropriate in many asymptomatic patients with elevated BPs while hospitalized, particularly in those with well-controlled BPs as outpatient (1-4). 

In a 2018 study involving > 14,000 older adults hospitalized for common non-cardiac conditions, 52% of the cohort with elevated BPs (majority ranging ~160-180 mm Hg) but well-controlled BPs at home were discharged on a more intensive antihypertensive regimen (1). Patients with history of MI or cerebrovascular disease were no more likely and those with limited life expectancy, dementia or metastatic cancer were no less likely to receive antihypertensive intensification which suggests the decision for more aggressive treatment of elevated BP was in large part driven by the BP readings themselves. 

More intensive anti-hypertensive therapy has not only been associated with lack of reduction in cardiac events or improvement in BP control following discharge but also with more adverse events, such as acute kidney injury, MI, falls, syncope and hypotension and increased risk of readmission (2-3). 

Another concern is the frequent use of IV antihypertensives with its attendant risk of overcorrection and adverse events. One study found that about one-third of patients with asymptomatic uncontrolled BP treated with IV antihypertensives had an excessive drop in BP of more than 25% within 6 hours (5).

Since many factors may contribute to transiently elevated inpatient BPs (eg,  acute pain, stress, anxiety, exposure to new drugs and white coat hypertension) (1), the best advice when dealing with an elevated BP in hospitalized patients may be to repeat the BP, gather data on home BPs, contextualize the findings based on likelihood of benefits and risks of more intensive therapy and discuss with the outpatient provider before discharging patients on more intensified anti-hypertensive therapy (4). 

Bonus Pearl: Did you know that nearly one-half of patients with well controlled BPs at home have hypertension during their hospitalization? (1)

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1. Anderson TS, Wray CM, Jing B, et al. Intensification of older adults’ outpatient blood pressure treatment at hospital discharge: national retrospective cohort study. BMJ 2018;362:k3503.

2. Anderson TS, Jing B, Auerback A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med 2019;170:1528-36.

3. Rastogi R, Sheehan MM, Hu B, et al. Treatment and outcomes of inpatient hypertension among adults with noncardiac admissions. JAMA Intern Med. Published online December 28, 2020.

4. Kearney-Strouse J. Tailor treatment for asymptomatic inpatient hypertension. ACP Hospitalist 2021; 15:22-23.

5. Lipari M, Moser LR, Petrovitch EA, et al. As-needed intravenous antihypertensive therapy and blood pressure control. J Hosp Med 2016;11:193-198.

6. Jacobs ZG, Najafi N, Fang MC, et al. Reducing unnecessary treatment of asymptomatic elevated blood pressure with intravenous medications on the general internal medicine wards: a quality improvement initiative. J Hosp Med 2019;14:144-150.

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!




Should I treat asymptomatic blood pressure (BP) elevation in my hospitalized patient with well-controlled BP prior to admission?

Can hypothyroidism be associated with hypertension?

Short answer: Yes! Just as hyperthyroidism, hypothyroidism is also associated with hypertension (1-5). Compared to normal subjects, patients with hypothyroidism have a 3-fold increased prevalence of hypertension, usually diastolic (2). In fact, hypothyroidism has been identified as a cause of hypertension in 3% of patients with high blood pressure and is the most common cause of secondary hypertension after renovascular hypertension (1-3).

High systemic vascular resistance and increased arterial stiffness are among the important mechanisms explaining hypothyroid-induced hypertension (1). High systemic vascular resistance is thought to be due to the absence of the vasodilator effects of T3 on vascular smooth muscle and decreased response to beta-adrenergic stimulation, which in turn leads to increased alpha-adrenergic responses. Increased arterial stiffness may also contribute due to the myxedema involvement of the arterial wall. Other potential factors include free water retention due to an inappropriate secretion of anti-diuretic hormone (ADH) and obesity in hypothyroid patients (1,4).

Similar to its prevalence in hypothyroidism, hypertension is about 3-fold higher in patients with overt hyperthyroidism compared to normal subjects (1). However, in contrast to hypothyroid patients, the hypertension in hyperthyroidism is primarily “cardiogenic”, where the increased blood pressure levels are mainly maintained by the increased cardiac output due to high stroke volume and heart rate (1).

Thus, both hypothyroidism and hyperthyroidism can be associated with hypertension!

Bonus pearl: Did you know that hypertension due to hypothyroidism is typically associated with a low-renin state, is particularly sensitive to salt intake, and may not respond as well to angiotensin -converting enzyme inhibitors (1)?

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1. Mazza A, Beltramello G, Armigliato M, et al. Arterial hypertension and thyroid disorders: what is important to know in clinical practice? Annales d’Endocrinologie 2011;72:296-303.
2. Dernellis J, Panaretou M. Effects of thyroid replacement therapy on arterial blood pressure in patients with hypertension and hypothyroidism 2002; Am Heart J 2002;143:718-24.
3. Anderson GH, Blakeman N, Steeten DHP. The effect of age on prevalence of secondary forms of hypertension in 4429 consecutively referred patients. J Hypertension 1994;12:609-15.
4. Saito I, ITO K, Saruta T. Hypothyroidism as a cause of hypertension. Hypertension 1983;5:112-15.
5. Chaker L, Bianco AC, Jonklaas J, et al. Hypothyroidism. Lancet 2017;390:1550-62.

Can hypothyroidism be associated with hypertension?

Should I consider acute acalculous cholecystitis in my elderly ambulatory patient admitted with right upper quadrant pain?

Short answer: Yes! Although we usually associate acute acalculous cholecystitis (AAC) with critically ill patients (eg, with sepsis, trauma, shock, major burns) in ICUs, AAC is not as rare as we might think in ambulatory patients. In fact, a 7 year study of AAC involving multiple centers reported that AAC among outpatients was increasing in prevalence and accounted for 77% of all cases (1)!

Although the pathophysiology of ACC is not fully understood, bile stasis and ischemia of the gallbladder either due to microvascular or macrovascular pathology have been implicated as potential causes (2). One study found that 72% of outpatients who developed ACC had atherosclerotic disease associated with hypertension, coronary, peripheral or cerebral vascular disease, diabetes or congestive heart failure (1). Interestingly, in contrast to calculous cholecystitis, “multiple arterial occlusions” have been observed on pathological examination of the gallbladder in at least some patients with ACC and accordingly a name change to “acute ischemic cholecystitis” has been proposed (3).

AAC can also complicate acute mesenteric ischemia and may herald critical ischemia and mesenteric infarction (3). The fact that cystic artery is a terminal branch artery probably doesn’t help and leaves the gallbladder more vulnerable to ischemia when arterial blood flow is compromised irrespective of the cause (4).

Of course, besides vascular ischemia there are numerous other causes of ACC, including infectious (eg, viral hepatitis, cytomegalovirus, Epstein-Barr virus, Salmonella, brucellosis, malaria, Rickettsia and enteroviruses), as well as many non-infectious causes such as vasculitides and, more recently, check-point inhibitor toxicity (1,5-8).

Bonus Pearl: Did you know that in contrast to cholecystitis associated with gallstones (where females and 4th and 5th decade age groups predominate), ACC in ambulatory patients is generally more common among males and older age groups (mean age 65 y) (1)?


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1. Savoca PE, Longo WE, Zucker KA, et al. The increasing prevalence of acalculous cholecystitis in outpatients: Result of a 7-year study. Ann Surg 1990;211: 433-37.
2. Huffman JL, Schenker S. Acute acalculous cholecystitis: A review. Clin Gastroenterol Hepatol 2010;8:15-22.
3. Hakala T, Nuutinene PJO, Ruokonen ET, et al. Microangiopathy in acute acalculous cholecystitis Br J Surg 1997;84:1249-52.
4. Melo R, Pedro LM, Silvestre L, et al. Acute acalculous cholecystitis as a rare manifestation of chronic mesenteric ischemia. A case report. Int J Surg Case Rep 2016;25:207-11.
5. Aguilera-Alonso D, Median EVL, Del Rosal T, et al. Acalculous cholecystitis in a pediatric patient with Plasmodium falciparum infection: A case report and literature review. Ped Infect Dis J 2018;37: e43-e45.  
6. Kaya S, Eskazan AE, Ay N, et al. Acute acalculous cholecystitis due to viral hepatitis A. Case Rep Infect Dis 2013;Article ID 407182.
7. Simoes AS, Marinhas A, Coelho P, et al. Acalculous acute cholecystitis during the course of an enteroviral infection. BMJ Case Rep 2013;12.
8. Abu-Sbeih H, Tran CN, Ge PS, et al. Case series of cancer patients who developed cholecystitis related to immune checkpoint inhibitor treatment. J ImmunoTherapy of Cancer 2019;7:118.



Should I consider acute acalculous cholecystitis in my elderly ambulatory patient admitted with right upper quadrant pain?

Why is my patient with diabetic ketoacidosis (DKA) and hypovolemia hypertensive?

Although we may expect patients with DKA to present with hypotension due to hypovolemia, many patients with DKA may actually be hypertensive. This finding is particularly intriguing because hyperinsulinemia, not insulinopenia as found in DKA, has been associated with hypertension. 1,2

Though not proven, potential explanations for hypertension in DKA include elevated serum levels of catecholamines, pro-inflammatory cytokines, renin, angiotension II and aldosterone.3-5 Hyperosmolality may also lead to the release of antidiuretic hormone (ADH) which increases blood pressure via V2 receptors.  Another possibility is that the high insulin levels associated with the treatment of DKA suppress the catecholamine-stimulated production of vasodilative eicosanoids (eg, prostaglandins) by adipose tissue. 1 It’s possible that in any given patient, 1 or more of these mechanisms may be enough to override the potential hypotensive effect of insulin deficiency in DKA.

We should note that reports of frequent hypertension in DKA have primarily involved pediatric patients. A 2011 study found that 82% of pediatric patients with DKA had hypertension during the first 6 hours of admission with no patient having hypotension.3  

On the other extreme, refractory hypotension without obvious cause (eg, sepsis, acute adrenal insufficiency, cardiogenic causes) has also been reported in DKA.5Because insulin inhibits the production of vasodilative prostaglandins (eg, PGI2 and PGE2), severe insulin deficiency in DKA can also contribute to hypotension along with volume depletion. 

Potential genetic polymorphism in the synthesis and metabolism of prostaglandins may at least partially explain the varied blood pressure response and whether a patient with DKA presents with hypertension or hypotension. 5  

The author would like to acknowledge the valuable contribution of Lloyd Axelrod MD, Massachusetts General Hospital, to this post.

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  1. Axelrod L. Insulin, prostaglandins, and the pathogenesis of hypertension. Diabetes 1991;40:1223-1227. 
  2. Chatzipantelli K, Head C, Megerman J, et al. The relationship between plasma insulin level, prostaglandin productin by adipose tissue and blood pressure in normal rats and rats with diabetes mellitus and diabetic ketoacidosis. Metabolism 1996;45:691-98. 
  3. Deeter KH, Roberts JS, Bradford H, et al. Hypertension despite dehydration during severe pediatric diabetic ketoacidosis. Pediatr Diabetes 2011;12:295-301. 
  4. Ferris JB, O’Hare JA, Kelleher CM, et al. Diabetic control and the renin-angiotensin system, catecholamines and blood pressure. Hypertension 1985 7(Suppl II):II-58-II-63.  
  5. Singh D, Cantu M, Marx MHM, et al. Diabetic ketoacidosis and fluid refractory hypotension. Clin Pediatrics 2016;55:182-84. 


Why is my patient with diabetic ketoacidosis (DKA) and hypovolemia hypertensive?