Hypertensive Emergency in the ED

Silvera Samson Raj

Second-year MRCEM Resident, Kauvery Hospital, Chennai, India

Abstract

Hypertension is a common chronic medical condition with around 30% prevalence in India. Around 1-2% of patients with hypertension develop a hypertensive crisis during their lifetime. Uncontrolled hypertension can progress to a hypertensive crisis defined as a systolic blood pressure >180 mmHg or a diastolic blood pressure >120 mmHg.

Hypertensive crisis can be further classified as a hypertensive urgency or hypertensive emergency depending on end-organ involvement including cardiac, renal, and neurologic injury.

Background

A hypertensive emergency is an acute, marked elevation in blood pressure (systolic >180 mmHg or/and diastolic >120 mmHg) that is associated with signs of end-organ damage. These can include the heart, lungs, kidneys, brain, and blood vessels. This case series emphasizes the pathophysiology, and fields a few case presentations of hypertensive emergencies, and highlights the role of the emergency department in its management.

Pathophysiology

Case 1

A 43-years-aged gentleman, known to have hypertension (on Telmisartan 40 mg twice daily) presented to the emergency room (ER) with history of head ache since previous day and afternoon, and nausea with drowsiness since the presenting day morning.

For the above-mentioned symptoms, he consulted outside the hospital where MRI brain was suggested and referred to our hospital for further management.

On initial evaluation at the ER:

General examination: Drowsy but arousable, afebrile, peripheries warm.

Airway: Patent, self-maintained.

Breathing: RR: 24/min; SpO2: 98% RA, normal vesicular breath sounds heard over both lungs.

Circulation: BP: 160/110mmHg; HR: 88/min; CVS: S1S2 heard, no murmurs heard, PA: soft, non-tender, bowel sounds heard.

Disability: GCS: E3V3M5 (11/15), Pupil bilateral 3 mm -equally reacting to light,

CBG: 115mg/dl.

	R	L
Power UL	4/5	5/5
LL	4/5	5/5
DTR	++	++
Tone	N	N
Plantar
Sensory	+	+

MRI Brain

(1) Intra-parenchymal bleed in left temporo-parietal region measuring 6.4 × 4 cm, with mass effect and midline shift by 2.9 mm.

(2) Bilateral fronto-parietal region sub-arachnoid bleed.

(3) Diffuse cerebral edema noted.

Case 2

A 71-years-aged gentleman, known hypertension (not on any regular medication), presented to ER with history of sudden onset of confused speech and disorientation for one day.

CT brain done outside showed no evidence of bleed.

On initial evaluation at ER:

General examination: conscious, confused speech, afebrile, peripheries warm.

Airway: Patent, self-maintained.

Breathing: RR; 20/min, SpO2; 97% RA, normal vesicular breath sounds heard over both lungs.

Circulation:

(a). BP; 160/100 mmHg, HR; 96/min, CVS; S1S2 normal, no murmurs heard.

(b). PA; soft, non-tender, bowel sounds heard.

Disability: GCS: E4V4M5 (14/15),

(a). Pupil bilateral 2 mm – equally reacting to light,

(b). Right hemineglect noted. No nystagmus.

(c). Extra ocular eye movements – full

(d). CBG: 97 mg/dl.

	R	L
Power UL	05-May	05-May
LL	04-May	05-May
DTR	++	++
Tone	N	N
Plantar	\| V	\| V
Sensory	+	+

MRI Brain (done here): Acute left parieto-temporal infarct.

Case 3

A 30-years-aged gentleman, known type 2 diabetes mellitus and hypertension, presented to ER with history of sudden onset of headache followed giddiness and vomiting 2 episodes containing food particles, projectile, non-blood stained, non-bilious. Patient also complained of inability to move left upper limb and lower limb since then.

On initial evaluation at the ER:

General examination: Drowsy but arousable, afebrile, peripheries warm.

Airway: Patent, self- maintained.

Breathing: RR: 19/min; SpO2: 99% RA, normal vesicular breath sounds heard over both lungs

Circulation:

(a). BP: 180/120 mmHg; HR: 62/min; CVS: S1S2 normal, no murmurs heard,

(b). PA: soft; non-tender, bowel sounds heard.

Disability: GCS: E3V5M6 (14/15),

(a). Pupil bilateral 3 mm equally reacting to light,

(b). No nystagmus, Extra ocular eye movements – full,

(c). Deviation of mouth to right side with loss of nasolabial fold on the left.

(d). CBG: 115 mg/dl.

R	L
Power UL	05-May	0/5
LL	05-May	0/5
DTR	++	++
Tone	N
Plantar
Sensory	+	+

CT Brain: Right massive intra cranial bleed with midline shift of 2 mm and mild mass effect.

Case 4

A 47-years-aged lady, known hypertension (off anti-hypertensives for 1 week), presented to ER with history of sudden onset of head ache – holocranial, associated with vomiting 2-3 episodes containing food particles, projectile, non-blood stained, non-bilious.

On initial evaluation at ER:

General examination: conscious, oriented, afebrile, peripheries warm.

Airway: Patent, self- maintained.

Breathing: RR: 17/min; SpO2: 98%; RA normal vesicular breath sounds heard over both lungs.

Circulation:

(a). BP: 160/100 mmHg; HR: 78/min; CVS-S1S2 normal, no murmurs heard,

(b). PA: soft; non-tender, bowel sounds heard.

Disability: GCS: E4V5M6 (15/15),

(a). Pupil bilateral 3 mm -equally reacting to light,

(b). No nystagmus, Extra ocular eye movements – full,

(c). CBG: 184 mg/dl.

	R	L
Power UL	05-May	05-May
LL	05-May	05-May
DTR	++	++
Tone	N	N
Plantar
Sensory	+	+

CT brain with cerebral angiogram:

(a). Small saccular aneurysm on anterior communicating artery.

(b). Acute sub-arachnoid hemorrhage in bilateral frontal, sylvian fissure, basal cisterns and inter hemispheric fissure noted.

(c). Intra-ventricular hemorrhage with diffuse cerebral edema.

Case 5

A 71-years-aged lady, known hypertension (not on any regular medication), presented to ER with history of spontaneous bleeding from right nostril, associated with lightheadedness and giddiness on postural change.

On initial evaluation at ER:

General examination: conscious, oriented, afebrile, peripheries warm.

Airway: Patent, self -maintained.

Breathing: RR: 15/min; SpO2: 98% RA; normal vesicular breath sounds heard over both lungs.

Circulation:

(a). BP: 170/100 mmHg, HR: 76/min; CVS-S1S2 normal, no murmurs heard,

(b). PA: soft, non-tender, bowel sounds heard.

Disability: GCS: E4V5M6 (15/15),

Discussion

Management of Hypertensive Emergency in the ED

Spontaneous intracerebral hemorrhage (ICH) secondary to hypertension has an overall annual incidence of â‰ˆ25 per 100 000. Early mortality is high (<=40% at 1 month) and increases <=60% at 1 year.

Non-traumatic intracranial bleeding (NTIB), comprising subarachnoid hemorrhage (SAH) and intra-cranial bleeding (ICH) is a significant public health concern [1]. Spontaneous intra-cerebral hemorrhage (ICH), which is defined as spontaneous rupture of the intra-cerebral small vessels following cerebral vessel wall degeneration due to chronic hypertension or rarely to cerebral amyloid angiopathy, has an incidence of 15-19/100,000/year and a 30-day mortality of 40-50%.

Acute in hospital mortality was 40%. Another 17% died during the long-term follow up, but none of them from cerebrovascular disease. Ninety-two percent of the survivors were ambulatory at follow up [2]. Aggressive pharmacological treatment of acute hypertension in patients with ICH can be initiated early with a low rate of neurological deterioration and hematoma expansion [2].

A multicenter prospective observational study was conducted to evaluate the feasibility and safety of intravenous antihypertensive protocol for acute hypertension in patients with intracerebral hemorrhage (ICH). Twenty-seven patients with ICH and acute hypertension (mean age 61.37 ± 14.27; 10 were men) were treated to maintain the systolic blood pressure (BP) below 160 mm Hg and diastolic BP below 90 mmHg within 24 h of symptom onset. Neurological deterioration (defined as a decrease in initial Glasgow Coma Scale score = 2) was observed in 2 (7.4%) of 27 patients during treatment. Among patients who underwent follow-up computed tomography, hematoma expansion (more than 33% increase in hematoma size at 24 h) was observed in 2 (9.1%) of 22 patients. Patients treated within 6 hours of symptom onset were more likely to be functionally independent (modified Rankin scale-= 2) at 1 month compared with patients who were treated between 6 and 24 hours (8 of 18 versus 0 of 9, P = .03) [2].

There was significantly greater decrease in the systolic, diastolic and MAP at the end of 30 min and one hour in the labetalol group compared with the nifedipine group. The reduction of MAP achieved within 30 min with labetalol was double that of nifedipine. Both oral nifedipine and intravenous labetalol are effective in the treatment of hypertensive crisis. Intravenous labetalol may have benefits because it is more effective in reducing the SBP, DBP and MAP to target levels with a lower number of doses [3].

Systolic blood pressure measurements are unreliable for the management of acute spontaneous intracerebral hemorrhage [4] there by an arterial line insertion for beat to beat monitoring of BP makes it more possible to aggressively treat the hypertension and achieve the target BP <140/90 mmHg in patients with ICH for better prognosis.

Tranexamic acid in non-traumatic intracranial bleeding: a systematic review and meta-analysis conducted in 2021 states that the sensitivity analyses confirmed benefits of TXA on mortality. TXA appears to be a therapeutic option to reduce non-traumatic intracranial bleeding mortality [5].

Effect of tranexamic acid in traumatic brain injury: a nested randomized, placebo-controlled trial (CRASH-2 Intracranial Bleeding Study) is established to reduce overall mortality [6]. The recommended dosage regimen is: 1-2 g intravenous bolus of tranexemic acid followed by 1 g 8th hourly (max 3-4 g per day) [6].

Conclusion

The take home points from this case series are:

(1) Early recognition and prompt imaging with aggressive control of blood pressure with target 140-150/90 mmHg in intra cranial bleeds reduces the mortality rate of patient. The earlier the recognition, better the prognosis.

(2) Use of intravenous beta blockers (labetelol) boluses followed by infusions instead of oral calcium channel blockers (nifedipine, amlodipine) will be helpful in reducing blood pressure in ER.

(3) Use of intravenous tranexemic acid in any kind of hemorrhage is an added advantage.

(4) Fundoscopy/Ophthalmoscope in ER is a handy equipment in early detection of hypertensive emergency and it plays a major role in recognizing early stages of hypertensive emergencies by ruling out papilledema.

(5) Securing an “Arterial line” will be a great asset in hypertensive crisis management by monitoring the accurate blood pressure. More than 20% decrease in mean arterial pressure within an hour can lead to tissue hypoperfusion. Hence management should be well balanced in both terms.

The way of presentation may be different in each scenario but without immediate management of hypertensive emergencies, it could lead to life-threatening and fatal outcomes. Expecting the worst possible outcome and acting accordingly is the key to approach. Poor compliance to regular medications is the basic cause of life-threatening situations. Prevention is always better than cure.

Acknowledgment

For constantly pushing and encouraging me to complete this case series, I would like to thank, Dr. Aslesha (Clinical lead- Emergency department), Dr. Niveanthini (Consultant- Emergency department), Dr. Vetri (Consultant- Emergency department), and Dr. Vidya (Consultant- Emergency department)

References

(1) Bouillon-Minois JB, Croizier C, Dutheil F. Tranexamic acid in non-traumatic intracranial bleeding: a systematic review and meta-analysis. Scientific Reports 2021;11:15275.

(3) Sathya Lakshmi B, Dasari P. FICOG; Oral nifedipine versus intravenous labetalol in hypertensive urgencies and emergencies of pregnancy: a randomized clinical trial. Obstet Med. 2012;5(4):171-175.

(4) Garg RK, Ouyang B, Zwein A. Systolic blood pressure measurements are unreliable for the management of acute spontaneous intracerebral hemorrhage. J Crit Care. 2022;70:154049.

(5) Chobanian A, Bakris G, Black H, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-72.

(6) Zampaglione B, Pascale C, Marchisio M, et al. Hypertensive urgencies and emergencies. prevalence clinical presentation. Hypertension. 1996;27:144-7.

Hypertensive Emergency in the ED