A Chicken-and-Egg Predicament: Malignant Hypertension Versus HIV-Induced Thrombotic Microangiopathic Anemia Conundrum.

Thrombotic microangiopathy (TMA) is a condition characterized by hemolytic anemia, thrombocytopenia, and organ damage due to the formation of microthrombi. It can be classified as primary or secondary, with secondary TMA being associated with conditions such as infections, autoimmune diseases, and malignancies. This report details the case of a 39-year-old male with secondary TMA, exploring the potential roles of malignant hypertension and HIV infection with the aim of examining the potential link between malignant hypertension and HIV infection in the development of TMA, highlighting the need for a thorough and broad diagnostic approach.

An audit for the inpatient management of patients with severe hypertension without acute end-organ damage at the Northern Sydney Local Health District.

Severe hypertension without acute end-organ damage is commonly encountered in inpatients. Despite this, there is a lack of international guidelines to manage this disorder. We conducted an audit to investigate the local practices within our health district. Current practices favour the use of rapidly acting antihypertensive drugs, which have been associated with iatrogenic injury.

von Hippel-Lindau Syndrome and Secondary Hypertension: A Case Report.

von Hippel-Lindau (VHL) syndrome (OMIM #193300) is an autosomal dominant disorder with incomplete penetrance occurring due to a mutation in the VHL gene present on chromosome 3. We present the case of a 21-year-old male with a history of retinoblastoma presenting with intermittent headaches for one month. He was a known hypertensive and his blood pressure on presentation was 180/100 mmHg. A secondary cause for his hypertension was sought. Multiple cysts in his pancreas, both his kidneys, and a mass in the right suprarenal fossa were detected on an abdominal ultrasonogram and a subsequent computed tomography scan of the abdomen. VHL and a pheochromocytoma were suspected, and a positron emission tomography-computed tomography scan was done which collaborated with the above findings. The presence of multiple cystic lesions in the pancreas and kidneys, especially in an individual with a family history of VHL syndrome, should alert the physician to the possibility of VHL syndrome. The need for evaluation of causes for hypertension, especially in young individuals with resistant hypertension, is also highlighted.

Blood pressure changes during ketamine infusion for the treatment of depression.

OBJECTIVE: This study aimed to examine blood pressure changes during ketamine infusion for depression and exploring the factors associated with these changes. METHOD: This study is a retrospective chart-review of patients with depression undergoing ketamine infusion at Yale Psychiatry Hospital during a 7-year period. Blood pressure (BP) was recorded every 10 min during the infusion. Surges in systolic and diastolic blood pressure (SBP, DBP), along with severe hypertension events, were analyzed in relation to patient demographics. RESULTS: A total of 138 patients received a total of 2342 infusions. SBP and DBP peaked at 40 min after the start of the infusion with a mean change of 16.0 (SD: 11.2) and 11.0 mmHg (SD: 8.45) respectively. Severe hypertension was observed in 17 patients (12.5%) and 23 infusion sessions (0.98%), occuring more frequently during the first three infusions (43.4%). Age (OR = 1.04 [1.02,1.05], p-value <0.001) was significantly associated with a surge in SBP and all patients with a past medical history of hypertension experienced a BP surge during their infusions. CONCLUSION: Ketamine infusions can cause significant blood pressure increases, particularly in older and hypertensive patients, highlighting the need for careful cardiovascular monitoring to mitigate risks during treatment.

High-Grade Atrioventricular Block Reveals Rare Transthyretin Cardiac Amyloidosis With Unique Hemodynamics.

Atrioventricular (AV) block is a common cardiac conduction disorder that is frequently encountered in clinical practice; however, the association with rare systemic conditions such as transthyretin amyloidosis (ATTR) is heavily underdiagnosed. ATTR amyloidosis is a systemic disorder characterized by the deposition of abnormal transthyretin protein fibrosis in various organs including the heart and vasculature, resulting in progressive organ dysfunction. We present a rare case of high-grade AV block unveiling ATTR cardiac amyloidosis with unusual hemodynamics, specifically severe supine hypertension with severe orthostatic hypotension. These findings posed a diagnostic challenge, underscoring the importance of a comprehensive diagnostic approach and meticulous review of medical history. Following pacemaker placement and the diagnosis of ATTR cardiac amyloidosis, our patient was started on a Tafamidis regimen.

Posterior Reversible Encephalopathy Syndrome With Hemorrhagic Transformation in the Postoperative Period of a Kidney Transplant.

Patients with end-stage renal disease (ESRD) who undergo kidney transplantation are at an increased risk of developing surgical and/or medical complications. Posterior reversible encephalopathy syndrome (PRES) is a rare complication that occurs in 0.34% of kidney transplant patients. It is characterized by a combination of neurological manifestations, risk factors, and characteristic radiological findings in neuroimaging studies. The development of PRES has been associated with various medical conditions and factors, including hypertension, the use of cytotoxic and immunosuppressive drugs, acute or chronic kidney disease, pre-eclampsia/eclampsia, autoimmune diseases, and solid organ and bone marrow transplantation. This report presents the case of a 19-year-old woman diagnosed with ESRD on hemodialysis due to lupus nephritis who experienced an episode of PRES with intraparenchymal hemorrhage during the postoperative period of kidney transplantation. The case emphasizes the importance of closely monitoring these patients during this period to enable early diagnosis and timely treatment of complications, ensuring a favorable prognosis.

Magnesium sulfate in preeclampsia: Broad indications, not only in neurological symptoms.

The role of magnesium sulfate for treatment of eclampsia is well established. The medication proved to be superior to other anticonvulsants to reduce the incidence of recurrent convulsions among women with eclampsia. Additionally, magnesium sulfate has been indicated for women with preeclampsia with different severe features. However, despite these recommendations, many clinicians are still not confident with the use of magnesium sulfate, even in settings with high incidence of preeclampsia and unacceptable rates of maternal mortality. This review brings basic science and clinical information to endorse recommendations to encourage clinicians to use magnesium sulfate for patients with all severe features of preeclampsia, not only for women with neurological symptoms. Additionally, other benefits of magnesium sulfate in anesthesia and fetal neuroprotection are also presented. Finally, a comprehensive algorithm presents recommendations to manage patients with preeclampsia with severe features between 34 and 36+6 weeks.

Furosemide to lower antenatal severe hypertension: a randomized placebo-controlled trial.

BACKGROUND: Hypertensive disorders of pregnancy are a leading cause of perinatal morbidity, and timely treatment of severely elevated blood pressure is recommended to prevent serious sequelae. In acute hypertension marked by increased blood volume, it is unknown whether diuretics used as an adjunct to antihypertensive medications lead to more effective blood pressure control. OBJECTIVE: This study aimed to evaluate whether the addition of intravenous furosemide to first-line antihypertensive agents reduces systolic blood pressure in acute-onset, severe antenatal hypertension with wide (≥60 mm Hg) pulse pressure. STUDY DESIGN: In this double-blinded randomized trial, participants received 40 mg of intravenous furosemide or placebo in addition to a first-line antihypertensive agent. The primary outcome was mean systolic blood pressure during the first hour after intervention. Secondary outcomes included corresponding diastolic blood pressure; systolic blood pressure, diastolic blood pressure, and pulse pressure at 2 hours after intervention; total reduction from qualifying blood pressure; duration of blood pressure control; need for additional antihypertensive doses within 1 hour; and electrolytes and urine output. A sample size of 35 participants per group was planned to detect a 15-mm Hg difference in blood pressure. RESULTS: Between January 2021 and March 2022, 65 individuals were randomized: 33 to furosemide and 32 to placebo. Baseline characteristics were similar between the groups. There was no difference in the primary outcome of mean 1-hour systolic blood pressure (147 [14.8] vs 152 [13.8] mm Hg; P=.200). We found a reduction in 2-hour systolic blood pressure (139 [18.5] vs 154 [18.4] mm Hg; P=.007) and a decrease in 2-hour pulse pressure (55 [12.5] vs 67 [15.1]; P=.003) in the furosemide group. Subgroup analysis according to hypertension type showed a significant reduction in 2-hour systolic blood pressure and 2-hour pulse pressure among patients with new-onset hypertension, but not among those with preexisting hypertension. Urine output was greater in the furosemide group, with no difference in electrolytes and creatinine before and after intervention. CONCLUSION: Intravenous furosemide in conjunction with a first-line antihypertensive agent did not significantly reduce systolic blood pressure in the first hour after administration. However, both systolic blood pressure and pulse pressure at 2 hours were decreased in the furosemide group. These findings suggest that a 1-time dose of intravenous furosemide is a reasonable adjunct to achieve blood pressure control, particularly in patients in whom increased volume is suspected.

Effects of intravenous nicardipine followed by oral labetalol in combination with nifedipine controlled-release tablet on severe peripartum hypertension.

OBJECTIVES: To investigate the effects of intravenous nicardipine as initial therapy and oral labetalol combined with nifedipine controlled-release tablet as subsequent treatment of severe peripartum hypertension. MATERIAL AND METHODS: Intravenous nicardipine was delivered as the initial treatment, after the target blood pressure (BP) had been achieved, oral labetalol was used to maintain the target BP. If oral labetalol failed to maintain the target BP, oral labetalol combined with nifedipine controlled-release tablet was used. RESULTS: A total number of 131 patients were enrolled. The target BP (BP < 140/90 mmHg) was achieved in all patients within 60 minutes by intravenous nicardipine. After receiving labetalol orally, the target BP was maintained in nine patients. However, in 104 patients, we had to combine oral labetalol and nifedipine controlled-release tablet due to re-elevation of their systolic BP to 140-159 mmHg. In 18 patients, we restarted intravenous nicardipine because their systolic BP re-elevated above 160 mm Hg. Among the 104 patients who received oral labetalol and nifedipine controlled-release tablet, the target BP was achieved and maintained in 96 patients, and eight patients had to restart nicardipine. Of the total number of 26 patients in whom intravenous nicardipine was resumed, the target BP was successfully maintained in 22 patients with oral labetalol combined with nifedipine controlled-release tablet. CONCLUSIONS: Intravenous nicardipine rapidly and safely lowered severe peripartum hypertension. As subsequent therapy, oral labetalol combined with nifedipine controlled-release tablet protocol may be applied to effectively maintain a target BP.

A Rare Case of Profound Sinus Bradycardia in a Patient With Descending Aortic Dissection.

A 34-year-old uncontrolled hypertensive male presented with chest pain radiating to the back. Despite severe pain, he was persistently bradycardic at 38 beats per minute. The workup at the emergency department confirmed the presence of an acute Stanford B aortic dissection. Stanford B dissections are not usually associated with bradycardia. It is Stanford A dissections that are mostly linked with bradycardia because Stanford A dissections can cause concomitant coronary artery extension and involvement of the atrioventricular node. This case demonstrates that sinus bradycardia can exist in the acute setting of any painful aortic dissection, even though it might not necessarily involve the coronary arteries.

Renin inhibition and the long-term renal function in patients with hypertensive emergency: a retrospective cohort study.

BACKGROUND: The rehospitalization rate in hypertensive emergency is high, indicating the necessity for optimizing its long-term management. The role of the renin-angiotensin system (RAS) blockade in this disorder remains uncertain. METHODS: We conducted a retrospective analysis involving 20 admitted patients who received aliskiren, a direct renin inhibitor (DRI), for the management of hypertensive emergency associated with elevated plasma renin activity (PRA). We analyzed the changes in blood pressure (BP), kidney function, and RAS activity in the subacute and chronic phases. RESULTS: The use of DRI was associated with a marked reduction in PRA (median, from 25.0 to 1.2 ng/mL/hr) and serum aldosterone levels (from 404 to 130 pg/mL) during the index admission. BP also decreased from 226/143 to 142/80 mmHg. A comparison of clinical characteristics according to the renal function indicated that dialysis-dependent patients had higher aldosterone levels than non-dialysis-dependent patients at admission, despite comparable BP levels. After a median follow-up of 567 days in non-dialysis-dependent patients with DRI, median eGFR levels were significantly increased from 14.3 to 23.1 mL/min/1.73 m2. PRA levels were consistently suppressed at 0.8 ng/mL/hr. We found a significant correlation between the degree of PRA suppression and changes in eGFR (r = -0.58), indicating that the effective blockade of RAS is associated with the preservation of eGFR in the study subjects. CONCLUSIONS: DRI can successfully suppress PRA in patients with high-renin hypertensive emergency in both subacute and chronic phases. An efficient RAS blockade is associated with preserved renal function in these patients.

Clinical utility of routine investigations and risk factors of end-organ damage in asymptomatic severe hypertension.

Asymptomatic severe hypertension is defined as systolic blood pressure of ≥ 180 mmHg or diastolic blood pressure of ≥ 120 mmHg without signs and symptoms of end-organ damage or dysfunction. Literature shows that around 5% of the patients with severe asymptomatic hypertension had acute hypertension-related end-organ damage. This study aimed to determine the clinical utility of routine investigations and risk factors of end-organ damage in patients presented to the emergency department with  asymptomatic severe hypertension. This single-center, cross-sectional study was conducted at the emergency department of the Aga Khan University Hospital, Karachi, Pakistan, from January 2018 to December 2020. All adult patients (age ≥ 18 years) presented to the emergency department with a systolic blood pressure of ≥ 180 or diastolic blood pressure of ≥ 120 mmHg without any signs and symptoms of end-organ damage (e.g., chest pain, unilateral limb or facial weakness, or hemiplegia, altered mental status, shortness of breath, decreased urine output, and sudden-onset of severe headache) were included. Routine investigations were analyzed to detect end-organ damage, including complete blood count, basic metabolic panel, urine detailed report, electrocardiogram, and troponin-I. Multivariable binary logistic regression was applied to identify the risk factors of end-organ damage considering the significant p value of ≤ 0.05. A total of 180 patients were presented to the emergency department with asymptomatic severe hypertension during the study period. Among the total patients, 60 patients (33.3%) had abnormal investigation findings; out of them, new-onset end-organ damage was diagnosed in 15 patients (8.3%). The most common end-organ damage was the kidney (73.3%) followed by the heart (26.6%). The multivariable binary logistic regression showed that age of more than 60 years, past medical history of diabetes, ischemic heart disease, and cerebrovascular accident were significantly associated with a higher risk of end-organ damage (p < 0.05). The study identified a higher prevalence of abnormal routine investigations and acute end-organ damage in emergency department patients with asymptomatic severe hypertension compared to high-income countries and suggested a lower threshold for end-organ damage screening in these patients. The current recommendations of foregoing further workup in patients with asymptomatic severe hypertension may need modification for emergency departments in low-middle-income countries if similar associations are replicated in other settings.

Comparing Intravenous Labetalol and Intravenous Hydralazine for Managing Severe Gestational Hypertension.

Background Hypertensive disorders of pregnancy are the leading causes of both maternal morbidity and maternal mortality. Hypertensive disorders are acute obstetric emergencies, which refer to various life-threatening medical challenges known to develop during pregnancy, labor, and delivery, requiring urgent attention to reduce blood pressure (BP) for the benefit of the affected mothers and infants. Hydralazine and labetalol have been widely used as the first-line medications in the management of severe hypertension during pregnancy. However, the choice between these two drugs lacks clear evidence regarding their safety and superiority. Several studies have attempted to study intravenous (IV) labetalol versus hydralazine, but very few such comparison studies have been conducted in Africa.  Objective To compare the effectiveness of IV labetalol and IV hydralazine in reducing systolic and diastolic BP in pregnant women with severe hypertension. Also, to determine the time required for hydralazine and labetalol to lower BP to ≤150/100 mmHg, the number of doses needed for each drug, and evaluating maternal and perinatal outcomes. Study design This study employed an open-label randomized clinical trial design conducted in the labor, delivery, and antenatal ward of the Central and Stella Obasanjo Hospital in Benin City. A total of 120 women with severe pregnancy-induced hypertension were randomly assigned to two groups: Group X, consisting of 60 pregnant women, received IV hydralazine at a slow rate of 5 mg for five minutes, repeated every 20 minutes (maximum of five doses) until a blood pressure of ≤150/100 mmHg was achieved. Group Y, also consisting of 60 pregnant women, received IV labetalol in escalating doses of 25, 50, 75, 75, and 75 mg (maximum of 300 mg) every 20 minutes until the blood pressure reached ≤150/100 mmHg. Statistical analysis was performed using SPSS version 23 (IBM Inc., Armonk, New York). Result IV hydralazine achieved the target BP in an average time of 45.80 +/- 25.17 minutes, while IV labetalol took an average of 72.67 +/- 41.80 minutes (p=0.001). The number of doses required to reach the target BP differed significantly between the two drugs. Hydralazine required an average of 1.72 +/- 0.904 doses, whereas labetalol required an average of 3.72 +/- 1.782 doses (p=0.0001). While 45% of women in the hydralazine group attained the target BP with a single dose of hydralazine, only 31.1% of women in the labetalol group were able to attain the target BP with a single dose of labetalol (p=0.02). Overall, target BP was achieved in 55 out of 60 women (91.7%) who were randomized to receive IV hydralazine, whereas 45 out of 60 women (75%) who received IV labetalol achieved the target blood pressure. While hydralazine demonstrated more favorable results in terms of achieving target blood pressure, there were higher incidences of maternal adverse effects in the hydralazine group compared to the labetalol group. However, these adverse effects were not severe enough to warrant discontinuation of the medication. Conclusion IV hydralazine showed faster achievement of the target BP and a lower number of doses required compared to IV labetalol. Additionally, a higher percentage of women in the hydralazine group achieved the target BP with a single dose. However, there were more maternal adverse effects associated with hydralazine, although they were not severe. Perinatal outcomes did not differ significantly between the two groups.

Severe hypertension development significantly improves progression-free survival in regorafenib treatment for metastatic colorectal cancer.

PURPOSE: Regorafenib is the first multikinase inhibitor used for metastatic colorectal cancer (mCRC) treatment. Reports regarding other multikinase inhibitors have suggested that the development of hypertension is associated with improved clinical benefits. We aimed to reveal the relationship between the development of severe hypertension and regorafenib efficacy in an mCRC real-world setting. METHODS: Patients with mCRC (n = 100) who received regorafenib were assessed retrospectively. The primary endpoint was a comparison of progression-free survival (PFS) between patients with and without ≥ grade 3 hypertension. The secondary endpoints were overall survival (OS), disease control rate (DCR), and adverse effects. RESULTS: Patients developing ≥ grade 3 hypertension accounted for 30%, and obtained significantly longer PFS than control patients (median PFS of 53 and 56 days, 95% confidence interval [CI] of 46-144 and 49-63 days, respectively; P = 0.04). In contrast, OS and DCR were not statistically different between the groups (P = 0.13 and P = 0.46, respectively). The incidence and severity of adverse effects were not significantly different, except for hypertension. Treatment interruption was significantly more frequent in patients with hypertension (P = 0.04). Multivariate Cox hazard analysis suggested that the development of ≥ grade 3 severe hypertension was an independent factor for improved PFS (adjusted hazard ratio 0.57, 95% CI 0.35-0.93; P = 0.02). In contrast, baseline hypoalbuminemia was associated with a worse PFS (1.85, 1.14-3.01; P = 0.01). CONCLUSION: We have revealed that patients who develop severe hypertension after regorafenib treatment for mCRC have improved PFS. Management of hypertension is important for effective treatment with less burden; therefore, further evaluation is needed.

Association between D-dimer and long-term mortality in patients with acute severe hypertension visiting the emergency department.

OBJECTIVE: High levels of D-dimer, a marker of thrombotic events, are associated with poor outcomes in patients with various cardiovascular diseases. However, there has been no research on its prognostic implications in acute severe hypertension. This study investigated the association between D-dimer levels and long-term mortality in patients with severe acute hypertension who visited the emergency department. DESIGN AND METHOD: This observational study included patients with acute severe hypertension who visited the emergency department between 2016 and 2019. Acute severe hypertension was defined as a systolic blood pressure ≥ 180 mmHg or a diastolic blood pressure ≥ 100 mmHg. Among the 10,219 patients, 4,127 who underwent D-dimer assay were analyzed. The patients were categorized into tertiles based on their D-dimer levels at the time of emergency department admission. RESULTS: Among the 4,127 patients with acute severe hypertension, 3.1% in the first (lowest) tertile, 17.0% in the second tertile, and 43.2% in the third (highest) tertile died within 3 years. After the adjustment for confounding variables, the third tertile of the D-dimer group (hazard ratio, 6.440; 95% confidence interval, 4.628-8.961) and the second tertile of the D-dimer group (hazard ratio, 2.847; 95% confidence interval, 2.037-3.978) had a significantly higher risk of all-cause mortality over 3 years than the first tertile of the D-dimer group. CONCLUSIONS: D-dimer may be a useful marker for identifying the risk of mortality among patients with acute severe hypertension who visit the emergency department.

Hypertensive Emergency As Initial Presentation of Systemic Sclerosis Sine Scleroderma.

Hypertensive emergency is a common cause of emergency room (ER) visits. Scleroderma renal crisis (SRC) is one of the rare causes of hypertensive emergency. SRC is a life-threatening condition that presents with acute onset severe hypertension accompanied by retinopathy, encephalopathy, and rapidly worsening renal function. We present a case of hypertensive emergency and renal failure with positive anti-Scl 70 and RNA polymerase III which is characteristic of SRC. Despite appropriate supportive care and timely treatment with angiotensin-converting enzyme inhibitors, the patient progressed to end-stage kidney disease.

Posterior Reversible Encephalopathy Syndrome in an Adult Male With Uncontrolled Blood Pressure and Cocaine Use: A Case Report.

Posterior reversible encephalopathy syndrome (PRES) is a subacute syndrome that is diagnosed by neurologic symptoms and radiologic findings. PRES is predominantly caused by uncontrolled hypertension though it has been associated with illicit drug use, specifically cocaine use. We describe a case of a 68-year-old male who developed visual disturbances and gait abnormalities. Imaging was confirmed with head CT that showed hypoattenuation in the posterior aspects of the occipital lobes. The patient was managed with anti-hypertensive medication and blood pressure monitoring during his hospital course. Therefore, the patient's neurological symptoms resolved once the blood pressure was well-controlled. MRI of the brain was completed prior to discharge and confirmed resolution. Hypertension and cocaine use has been documented as causative agents of PRES. It is most likely due to the inability of the posterior circulation of the brain to auto-regulate with acute changes in blood pressure resulting in hypoperfusion and disruption of the blood-brain barrier with resultant vasogenic edema without infarction.

Genetic, clinical, and pathological study of patients with severe hypertension-associated renal microangiopathy.

BACKGROUND: Severe hypertension may be a prominent manifestation of complement-mediated thrombotic microangiopathy. Furthermore, patients with severe hypertension-associated thrombotic microangiopathy may present with concurrent hematologic abnormalities that mimic complement-mediated thrombotic microangiopathy. Whether or not severe hypertension-associated thrombotic microangiopathy is associated with genetic susceptibility in complement- and/or coagulation-pathway genes remains unclear, and there is thus a need to identify clinicopathological clues to distinguish between these entities. METHODS: Forty-five patients with concomitant severe hypertension and thrombotic microangiopathy on kidney biopsy were identified retrospectively. Whole-exome sequencing was performed to identify rare variants in 29 complement- and coagulation-cascade genes. Clinicopathological features were compared between patients with severe hypertension-associated thrombotic microangiopathy and complement-mediated thrombotic microangiopathy with severe hypertension. RESULTS: Three patients with pathogenic variants diagnostic of complement-mediated thrombotic microangiopathy and two with anti-factor H antibody positivity were diagnosed with complement-mediated thrombotic microangiopathy with severe hypertension. Among the 40 patients with severe hypertension-associated thrombotic microangiopathy, 53 rare variants of uncertain significance were found in the analyzed genes in 34 (34/40, 85%) patients, of whom 12 patients harbored two or more variants. Compared with complement-mediated thrombotic microangiopathy patients with severe hypertension, patients with severe hypertension-associated thrombotic microangiopathy were more likely to have left ventricular wall thickening (p < 0.001), less-severe acute glomerular thrombotic microangiopathy lesions including mesangiolysis and subendothelial space widening (both p < 0.001), and less arteriolar thrombosis formation (p < 0.001). CONCLUSIONS: Rare genetic variants involving complement and coagulation pathways can be found in patients with severe hypertension-associated thrombotic microangiopathy; their role needs further investigation. Cardiac remodeling and acute glomerular TMA lesions may help to differentiate between severe hypertension-associated thrombotic microangiopathy and complement-mediated thrombotic microangiopathy with severe hypertension.

Managing severe hypertension in children.

Severe childhood hypertension is uncommon and frequently not recognised and is best defined as a systolic blood pressure (SBP) above the stage 2 threshold of the 95th centile + 12 mmHg. If no signs of end-organ damage are present, this is urgent hypertension which can be managed by the slow introduction of oral or sublingual medication, but if signs are present, the child has emergency hypertension (or hypertensive encephalopathy if they include irritability, visual impairment, fits, coma, or facial palsy), and treatment must be started promptly to prevent progression to permanent neurological damage or death. However, detailed evidence from case series shows that the SBP must be lowered in a controlled manner over about 2 days by infusing short-acting intravenous hypotensive agents, with saline boluses ready in case of overshoot, unless the child had documented normotension within the last day. This is because sustained hypertension may increase pressure thresholds of cerebrovascular autoregulation which take time to reverse. A recent PICU study that suggested otherwise was significantly flawed. The target is to reduce the admission SBP by its excess, to just above the 95th centile, in three equal steps lasting about ≥ 6 h, 12 h, and finally ≥ 24 h, before introducing oral therapy. Few of the current clinical guidelines are comprehensive, and some advise reducing the SBP by a fixed percentage, which may be dangerous and has no evidence base. This review suggests criteria for future guidelines and argues that these should be evaluated by establishing prospective national or international databases.

Diffuse Alveolar Hemorrhage: A Rare Complication of Severe Hypertension.

Severe hypertension is a rare cause of diffuse alveolar hemorrhage. We reported a case of a 43-year-old woman who presented with shortness of breath, hemoptysis, and severe hypertension. The patient was diagnosed with diffuse alveolar hemorrhage due to severe hypertension which improved after controlling her blood pressure.