Pearls
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Acute severe hypertension, defined as significant blood pressure (BP) elevation with or without evidence of acute hypertensive target-organ damage, requires prompt therapy to prevent and/or ameliorate further target-organ damage.
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The most common causes of acute severe hypertension in children are renal and cardiac conditions. The central nervous system is the most commonly affected target organ.
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Mechanisms of acute severe hypertension may include volume overload with or without renal dysfunction and/or activation of the renin-angiotensin-aldosterone system.
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Treatment of acute severe hypertension requires continuous monitoring of BP and administration of intravenous antihypertensive medication(s), most commonly labetalol or nicardipine.
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Mean arterial pressure in patients with acute severe hypertension and significant target-organ involvement should be lowered no more than 25% within the first 8 hours to prevent harm from dropping BP and thus organ perfusion too rapidly (e.g., cerebral, coronary, or renal ischemia).
Primary (sometimes referred to as essential) hypertension (HTN) is a relatively uncommon condition in children and adolescents, with an estimated prevalence of 3% to 5%. The prevalence has increased over the past 2 decades as a consequence of the childhood obesity epidemic and is likely to be diagnosed more often because of recent changes in the normative data used to define childhood HTN (see later discussion). While most hypertensive patients in the pediatric intensive care unit (PICU) will have secondary HTN (i.e., HTN because of another underlying condition), the increasing prevalence of pediatric primary HTN may ultimately increase the frequency that such patients present to the PICU.
Several questions are commonly posed to the intensivist when managing a patient with acute severe HTN. What constitutes acute severe HTN in the PICU? Is this level of HTN dangerous? Does the HTN represent a transient acute response or is there an underlying chronic process to be uncovered? Is it important to manage the high blood pressure (BP) at this moment? How aggressively should it be managed? This chapter promotes understanding of the deleterious effects of severe HTN, recognition of when invasive versus noninvasive monitoring is warranted, and development of a prompt but cautious approach to management.
Terminology
The most recent clinical practice guidelines for diagnosing and managing HTN in children and adolescents were published in 2017 by the American Academy of Pediatrics (AAP). They were designed to align with adult guidelines from the American Heart Association and American College of Cardiology, which were also released in 2017. By using a statistical definition based on the distribution of BP values in the pediatric population, HTN in children and adolescents is defined as sustained systolic and/or diastolic BP elevation greater than or equal to the 95th percentile for age, gender, and height, with adult BP cutpoints used in adolescents aged 13 years or older. Its severity can be further classified according to the scheme in Table 78.1 . Of note, the 2017 AAP guideline calls out BP readings greater than 30 mm Hg above the 95th percentile as being potentially associated with a risk of development of acute complications of HTN.
| Blood Pressure Classification | Children and Adolescents <13 Years | Adolescents ≥13 Years |
|---|---|---|
| Normal | SBP and DBP <90th percentile | SBP <120 mm Hg and DBP <80 mm Hg |
| Elevated blood pressure | SBP or DBP 90th–95th percentile, or if BP is 120/80 to <95th percentile | SBP 120–129 mm Hg and DBP <80 mm Hg |
| Stage 1 hypertension | SBP or DBP ≥95th–95th percentile plus 12 mm Hg, or if BP is 130/80 to 139/89 mm Hg | SBP 130–139 mm Hg or DBP 80–89 mm Hg |
| Stage 2 hypertension | SBP or DBP >95th percentile plus 12 mm Hg, or if BP is ≤140/90 | SBP ≥140 mm Hg or DBP ≥90 mm Hg |
Severe HTN, however, has not been as rigorously defined, which has led to some confusion with respect to terminology. The clinical state of a “malignant sclerosis” or “bösartig hypertension” was first reported by Volhard and Fahr in 1914 in patients with HTN and “hypernephrosclerosis.” In 1928, Keith et al. described 81 cases of what was termed “the malignant hypertension syndrome,” which was a diagnosis made before end-stage damage of retinal, cerebral, cardiac, or renal function occurred. , It was also the first description of pediatric patients with significantly uncontrolled HTN. Subsequently, the terms hypertensive crisis and hypertensive emergency have appeared interchangeably in the literature, usually to denote a rapidly elevated level of either systolic or diastolic BP that is associated with end-organ damage. A preferred term, acute severe hypertension , denotes this potentially dangerous condition; the terms hypertensive emergency and hypertensive urgency may be used to differentiate between levels of target-organ involvement (see later discussion). Acute severe HTN can be defined as an acute BP elevation that fulfills (and usually exceeds) the definition of stage 2 HTN and that is accompanied by severe symptoms. Physical examination and/or laboratory findings of accelerated HTN are frequently also present.
Organs commonly affected by acute severe HTN include the central nervous system (CNS) (hypertensive encephalopathy, retinal vasculopathy–induced visual changes, cerebral infarction, and hemorrhage); the cardiovascular system (congestive heart failure, myocardial ischemia, aortic dissection); and the kidneys (proteinuria, hematuria, and acute renal insufficiency).
Traditionally, severe HTN has been divided into hypertensive emergencies and hypertensive urgencies, the former associated with life-threatening symptoms and/or target-organ injury and the latter associated with less significant symptoms and no target-organ injury. , For example, an adolescent with seizures and hypertensive encephalopathy would be considered to be experiencing a hypertensive emergency, whereas a hypertensive child with nausea and vomiting would be classified as a hypertensive urgency. This distinction is not absolute and depends on clinical judgment.
Etiology
HTN may be either primary (essential) or secondary to another underlying medical condition. Children with primary HTN are frequently overweight and have positive family histories for HTN and cardiovascular disease. The prevalence of primary pediatric HTN increases progressively with increasing body mass index, with approximately 30% of overweight children (body mass index >95th percentile) exhibiting HTN. That said, although the frequency of primary HTN has been increasing, it is unusual in the PICU, with almost all cases of acute severe HTN being secondary to another condition.
Secondary causes of HTN can either be transient or sustained. The most common reasons for transiently elevated BP in a critical care unit are inadequately treated pain and agitation. Without a high degree of suspicion, this can be difficult to detect, particularly if neuromuscular blockade is administered. Tachycardia and eye tearing with noxious interventions are two useful clues to this condition. Drug-induced HTN is also common in the critical care setting, especially when high-dose corticosteroids are administered to patients with organ transplantation and other immunologic conditions. A number of other drugs associated with elevated BP are listed in Box 78.1 . Reviewing all medications taken by the patient and considering the possibility of illicit drug use is therefore necessary in all patients with a significantly elevated BP. A patient’s fluid balance should also be reviewed when HTN develops while in the ICU. Apparently innocuous daily discrepancies between input and output can cumulatively produce significant fluid overload after several days, although this alone is not typically enough to cause acute severe HTN in the absence of other renal, cardiovascular, or CNS problems. Finally, postoperative HTN is common in the ICU setting, occurring in up to 75% of patients. Initially, factors such as hypoxia, hypercarbia (through its sympathomimetic effects), and pain should be promptly and adequately addressed. Afterward, pharmacologic therapy is indicated if HTN is refractory or sustained despite adequate ventilation, sedation, and analgesia.
Renal disease predominates in most pediatric case series of acute severe HTN ( Box 78.2 ). Deal et al., from Great Ormond Street Hospital, retrospectively reviewed their experience with severe HTN in children in 1992. The most common causes of severe HTN in their series included reflux nephropathy, glomerular disease, renovascular disease, obstructive uropathy, and hemolytic-uremic syndrome, which together accounted for 76% of the cases. In a relatively large series of children with severe HTN treated with intravenous (IV) nicardipine, causes included complications of organ transplantation, multiorgan failure, renovascular disease, and acute kidney injury (AKI). Renal disease accounted for 48% of patients included in a more recent case series focusing on the use of IV labetalol in severely hypertensive infants. Cancer complications and renal disease were the most common conditions associated with hypertensive crisis in a case series from South Korea that likely reflects the patient population seen in most tertiary centers.
Renal disease
Glomerulonephritis (GN), especially membranoproliferative GN
Reflux nephropathy
Obstructive uropathy
Acute kidney injury
Polycystic kidney disease
Hemolytic-uremic syndrome
End-stage renal disease at presentation
Vascular
Aortic coarctation (thoracic, abdominal)
Renal artery stenosis
Vasculitis
Malignancy
Pheochromocytoma
Wilms tumor
Neuroblastoma
Other
Medication noncompliance in a patient with known hypertension
Drug-induced (see Box 78.1 )
• Box 78.1
Drug-Induced Hypertension
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Drug withdrawal (narcotic, benzodiazepine) a
a More likely to present acutely.
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Cyclosporine and tacrolimus a
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Erythropoietin
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Glucocorticoids and mineralocorticoids
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Heavy metals
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Maternal drug use (cocaine, heroin)
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3,4-methylenedioxymethamphetamine (“ecstasy”) a
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Nonsteroidal antiinflammatory agents
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Oral contraceptive agents
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Rebound after withdrawal of antihypertensives (especially clonidine, methyldopa, and β-blockers) a
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Sympathomimetic drugs (amphetamines, cocaine, ephedrine, lysergic acid diethylamide, phenylephrine) a
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Theophylline/caffeine
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Primary hypertension (rare)
Severe fluid overload in dialysis patients or noncompliance with antihypertensive therapy in patients with established HTN of any cause may also result in severe, symptomatic HTN requiring immediate treatment. This was clearly demonstrated in a case series of adults presenting to the emergency department of a teaching hospital in the United States. In that study, 90% of patients requiring intervention for a hypertensive urgency had a known diagnosis of HTN; the most common contributing factors to the severe BP elevation included running out of prescribed medications and medication noncompliance. While no similar pediatric data exist, anecdotal experience suggests that similar acute presentations with severe HTN may occur in chronically hypertensive children and adolescents followed at referral centers. Finally, abrupt withdrawal of either clonidine or a beta-adrenergic blocker may result in severe “rebound” HTN that may require prompt intervention.
Pathophysiology
The mechanisms responsible for generating and maintaining acute severe HTN continue to be elucidated. What seems plausible in many cases is that there is a triggering event that precipitates a dramatic increase in BP over a short time period in a patient who is hypertensive at baseline. This event then leads to further arteriolar damage that prolongs the hypertensive state.
Mean arterial pressure (MAP) is approximately equal to the product of cardiac output (CO) and systemic vascular resistance (SVR), as expressed mathematically as MAP ≅ CO × SVR. (Central venous pressure should be subtracted from the MAP in this equation but is usually so small it can be ignored.) Thus, factors that increase either CO or SVR lead to elevated BP if the other does not decrease proportionally. In addition, chronically, these factors have an interdependent interaction that is still poorly understood. For example, while the initiating event leading to HTN may cause a rise in CO, a compensatory rise in peripheral vascular resistance often develops that may persist even after CO returns to baseline.
Endothelial homeostasis
The endothelium seems to play a crucial role in the development of severe symptomatic HTN. The endothelium is on the receiving end of the excessive pressures and shear stress generated from high blood flows along with concomitant increased resistance imparted by the vascular architectural scaffolding and surrounding smooth muscle cells (see also Chapter 23 ). Aside from structural trauma, endothelial cell function is also affected. For instance, the stressed endothelial cell increases intracellular levels of nuclear factor-κB (NF-κB). In turn, NF-κB leads to generation of inflammatory mediators that lead to endothelial dysfunction and vascular injury. ,
Adults with primary HTN who experienced acute severe HTN demonstrated a significant decline in BP when given l -arginine (a precursor of nitric oxide [NO]) compared with patients who also had primary HTN but had not experienced a similar event. This observation underscores the importance of the endothelium in the pathogenesis of acute severe HTN because an intact functional endothelial cell surface is necessary to respond to l -arginine. Von Willebrand factor (an endothelial cell surface marker), P-selectin (platelet activation), and fibrinogen serum levels were all increased in hypertensive adult patients with acute severe HTN compared with control hypertensive subjects, suggesting that alterations in the homeostasis of the endothelial and/or the coagulation system occur during an episode of acute severe HTN.
Sympathetic nervous system activation
A common cause of increased CO in hypertensive individuals is sympathetic nervous system (SNS) activation, often in concert with an increase in intravascular volume. At the same time, SNS activation further increases SVR, exacerbating the rise in BP. The therapeutic approach to HTN depends on reducing SVR and often suppressing or reducing SNS activation. Without the latter being suppressed, the drop in SVR mediated by a vasodilator may be compensated by an increase in sympathetic activation, with a resultant increase in CO and no net reduction in BP.
The SNS can also be the cause of severe HTN. This is particularly seen in children with pheochromocytomas and other tumors that produce vasoactive substances, including neuroblastoma. End-stage kidney disease is characterized by SNS activation, which can contribute to a substantial increase in catecholamines and renin, which then can contribute to HTN. Increased SNS activity can worsen severe HTN in several conditions, including renovascular HTN and polycystic kidney disease, and seems to be unrelated to the level of kidney function. Renal ischemia triggered by these diseases seems to cause the systemic overactivation. Activation of the SNS leading to systemic vasoconstriction is generally accepted as the mechanism of severe postoperative HTN.
Renin-angiotensin-aldosterone system
The renin-angiotensin-aldosterone system (RAAS) plays a prominent role in many patients with acute severe HTN. , Renin is a proteolytic enzyme synthesized in the juxtaglomerular cells of the afferent renal arterioles that cleaves angiotensinogen (an α 2 -globulin synthesized in the liver) to create angiotensin I (a decapeptide). In turn, angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II (an octapeptide), which acts at the angiotensin type 1 receptor (a G-coupled receptor found in renal afferent and efferent arterioles) to cause vasoconstriction, increased aldosterone release, and enhanced sodium and water reabsorption.
Increased serum renin levels can reflect a primary condition, such as renovascular disease, or can be secondary to renal parenchymal ischemia, hypotension, hypovolemia, increased sympathetic effects, β-adrenergic agonists, or a combination of these factors. , Ultimately, increased renin levels raise BP through a number of mechanisms primarily mediated through angiotensin II. Aside from its vasoconstrictive properties, angiotensin II increases the expression of aldosterone that leads to increased renal sodium and water retention, thus augmenting CO by increasing intravascular volume. Angiotensin II also induces the expression of interleukin-6 and NF-κB; this, in turn, leads to elevated levels of tumor necrosis factor-α and increases nicotinamide adenine dinucleotide phosphate oxidase activity. The latter initiates generation of reactive oxygen species, promoting oxidative stress, and inhibits the cytokine-mediated activation of inducible-nitric oxide synthase (iNOS) that attenuates vasodilation. Over time, the collective result of these processes is enhanced and sustained endothelial cell trauma, vascular dysfunction, and ultimately, end-organ damage.
Nitric oxide
NO, now recognized as a ubiquitous biological effector, is a labile, short-lived chemical produced from arginine via NO synthases. These synthases are distinguished by cellular distribution and by the requirement for calcium as a cofactor. The constitutive isoform of NOS is believed most responsible for basal vasomotor tone, although iNOS may have a role. NO is released continuously from arteries and arterioles but not from veins. In addition, other mediators function through the NO system. For instance, bradykinin stimulates the release of NO to produce vasodilation. NO diffuses from the endothelium to the vascular smooth muscle cell, where it produces its vasodilatory effect in part by increasing the intracellular concentration of cyclic guanosine monophosphate (cGMP) through stimulation of soluble guanylate cyclase. NO that diffuses from the local endothelial environment reacts with hemoglobin, forming nitrosohemoglobin and methemoglobin. Thus, HTN need not be attributed only to a direct vasoconstrictor effect but also may be related to loss of basal NO vasodilation. Antihypertensive drugs used in acute severe HTN, such as sodium nitroprusside and nitroglycerin, produce their systemic vasodilator action by stimulating NO production (see HTN management section that follows).
Volume overload
An acute increase in intravascular volume is a frequent cause of acute decompensation of BP control in a patient with chronic HTN, particularly in the setting of stimuli that increase SNS and/or RAAS activation. Volume overload is the most common mechanism leading to HTN in children with renal diseases. It is often caused by AKI with oliguria or anuria in those without preexisting renal disease.
Although volume overload is a common cause of acute severe HTN, pressure diuresis may render some patients relatively hypovolemic, producing hemoconcentration and further marked activation of the RAAS. Further volume depletion may actually worsen HTN by stimulating a further increase in SVR with the potential for organ ischemia. Thus, diuretics and fluid restriction are not standard therapy for most patients who present with acute severe HTN; they are reserved for patients with clinically apparent fluid overload. ,
One patient population in whom fluid overload is probably the most important contributing factor to episodes of severe HTN are children and adolescents on dialysis. Fluid overload in dialysis patients most often results from poor adherence to dietary sodium and fluid restriction. Chronic underdialysis and failure to consistently reach “dry weight” may lead to gradual fluid accumulation that can be clinically imperceptible until the child presents with acute severe HTN. This may happen even in the best dialysis center due to the difficulty in assessment of fluid status in children and because differences in body weight may be attributed to growth instead of to fluid accumulation.
Clinical presentation
The presentation of a patient with acute severe HTN depends on underlying medical conditions, baseline systemic BP, rate of rise and degree of BP elevation, and effects on end organs. Headache, dizziness, and nausea/vomiting are common presenting complaints in patients with acute severe HTN, as was recently demonstrated in two pediatric case series of patients with acute severe HTN. , Visual impairment is another common presenting complaint in patients with acute severe HTN and may signal the presence of CNS involvement. A small number of severely hypertensive children may manifest isolated abdominal pain with or without vomiting. Although exceedingly rare in the pediatric age group, aortic dissection may present with severe HTN along with the abrupt onset of chest or back pain.
Neurologic manifestations of acute severe HTN are probably most common in children. Symptoms may include seizures, lethargy, confusion, headache, and visual disturbances, especially cortical blindness. Hypertensive encephalopathy (increased blood flow with pressures exceeding the autoregulatory range) typically presents as a severe headache with dizziness and changes in mental status ultimately culminating as seizures. Other reported symptoms include facial palsies and visual changes that may lead to blindness and coma. , , Hypertensive encephalopathy may occur with a MAP below 200 mm Hg in the normotensive individual, but it may require a much higher MAP in patients who have sustained HTN ( Fig. 78.1 ).
Cardiac manifestations of severe acute HTN can also be seen in children, although not as often as in adults. These may include asymptomatic left ventricular hypertrophy, acute congestive heart failure with pulmonary edema, and myocardial ischemia. , In two case series of children with severe HTN from the Great Ormond Street Hospital, the incidence of left ventricular hypertrophy ranged from 13% to 66%, and the incidence of congestive heart failure was 9%. , Clearly, a high index of suspicion for an underlying cause of HTN should be maintained in a patient who presents acutely with cardiac symptoms and severe HTN and appropriate investigation initiated.
Severely hypertensive children can also exhibit evidence of AKI, such as hematuria, albuminuria, and azotemia. However, in many cases, attempts to determine the acute renal effects of severe HTN may be complicated by the frequent association of renal parenchymal and/or renovascular disease with systemic HTN in children. Moreover, hypertensive pathology is not usually limited to a single organ like the kidney; other end-organ abnormalities usually can be seen, such as left ventricular hypertrophy and neurologic sequelae (such as mental status changes, seizures, and cerebrovascular accidents). Nevertheless, children with severe HTN resulting from vasculitis have been found to have nephrotic range proteinuria, microscopic hematuria, elevated serum creatinine levels, and diminished glomerular filtration rates.
Patient evaluation and monitoring
Blood pressure measurement and other monitoring
The most critical component of identifying and monitoring patients with acute severe HTN is accurately measuring BP. Both noninvasive and invasive techniques may be used in the ICU setting and are commonly used together. The main techniques available to determine BP in the ICU are the auscultatory method, oscillometric method, Doppler method, and invasive hemodynamic monitoring.
Auscultatory, oscillometric, and Doppler BP methods are noninvasive techniques that are based on the return of blood flow through a major artery after compression by an inflatable cuff. Auscultatory methods require the observer to listen to the Korotkoff sounds generated as the sphygmomanometer cuff deflates. Korotkoff sounds 1 and 5 should be used to represent systolic blood pressure (SBP) and diastolic blood pressure (DBP), respectively. It should be noted that the current pediatric normative BP values were generated using this technique over the brachial artery; therefore, it is the preferred site of BP measurement in children and adolescents. To obtain accurate measurements, it is important that an appropriately sized cuff size be used, which should cover 80% to 100% of the upper arm circumference. Although auscultation can be time-consuming, it can be helpful to confirm BP values obtained by other methods.
Oscillometric techniques use a similar technique except that the MAP is first determined from oscillometric wave forms generated as blood flow returns through the artery. SBP and DBP are then calculated using a proprietary formula specific to the brand of monitor. Oscillometric methods are known to overestimate both SBP and DBP, but since the devices can be programmed to take repeated BP measurements at regular intervals, they can provide vital information regarding BP trends.
Doppler devices use changes in ultrasound frequency to infer velocity of blood flow. The Doppler shift corresponds to the turbulent flow, as signified by the Korotkoff sounds, that diminishes as laminar flow predominates. As with the auscultatory method, selection of an appropriate cuff size is paramount for both the oscillometric and Doppler BP methods.
Invasive arterial lines are fluid-filled tubes attached to a pressure transducer—a device consisting of a thin, flexible diaphragm connected to a strain gauge and capable of converting the pressure transmitted to an electrical signal (see Chapter 26 ). The most common source of inaccuracy is the influence of electrical damping on reported BP. An overdamped signal underestimates both SBP and DBP, although MAP may be accurate. On the other hand, an underdamped system overestimates SBP, especially with a hyperdynamic circulation, but does not affect MAP. This phenomenon is recognized as a narrow-peaked pressure wave and wide pulse pressure. Moreover, invasive BP measured in the lower extremity is higher than in the upper extremities because of the nature of BP wave transmission, which results in an increase in SBP reading the farther away from the heart it is measured.
Generally, children with acute severe HTN need to be closely monitored in a controlled setting, such as the ICU, and the ideal way to continuously follow BPs is with the aid of an indwelling arterial catheter. Arterial lines can be placed in a variety of locations, but usually they are placed in peripheral arteries that supply areas with robust collateral blood flow. Common sites include the radial, dorsalis pedis, and posterior tibial arteries. Continuous intraarterial BP monitoring is generally preferred for patients with acute severe HTN because of the lability of BP when continuous infusions of IV medications are used. However, using noninvasive techniques to confirm that transduced values are accurate is a quite common practice because electrical damping of the transduced signal can cause inaccuracies in SBP and DBP, although MAP is likely to be less affected. Additionally, as mentioned previously, modern oscillometric devices can be programmed to take repeated measurements of BP at short intervals. Therefore, they may sometimes be acceptable for short time periods or for patients without life-threatening symptoms.
Other important aspects of monitoring the patient with acute severe HTN include pulse oximetry and frequent neurologic assessment. Appropriate IV access should be established; ideally, there should be an IV line placed that is used only for administration of antihypertensive medications. Monitoring of central venous pressure may also be helpful in selected patients, especially when volume status is otherwise difficult to assess. A central line may also be needed for administration of intravenous antihypertensive medications, such as nicardipine. Finally, an indwelling Foley catheter may be needed for urine output monitoring, especially in severely hypertensive patients with known or suspected acute or chronic kidney disease.
Diagnostic evaluation
Evaluation should be targeted at identifying underlying etiology and potential signs of injury to the cardiovascular, nervous, renal, and ocular systems. A detailed history and review of systems should be obtained for all patients, with special care paid to symptoms suggestive of an underlying hypertensive disorder or target-organ damage ( Table 78.2 ). Signs and symptoms often reflect severity and rapidity of onset of HTN. Chronic HTN is more commonly asymptomatic or characterized by low-grade generalized symptoms such as fatigue and recurrent headaches. As already discussed, acutely hypertensive patients may present with a wide range of symptoms, with headache, nausea, seizures, and other neurologic complaints among the most common.
| Finding | Possible Significance |
|---|---|
| Historical Findings | |
| Complaint/Review of Systems | |
| Headaches, dizziness, epistaxis, visual changes | Nonspecific with respect to etiology of HTN |
| Abdominal/flank pain with hematuria | Renal artery or vein thrombosis |
| Hematuria, swelling, decreased urine output | Acute glomerulonephritis |
| Dysuria, frequency, urgency, nocturia, enuresis | Underlying renal disease |
| Joint pains/swelling, edema, rashes | Autoimmune-mediated disease/glomerulonephritis |
| Weight loss, sweating, flushing, palpitations | Pheochromocytoma or hyperthyroidism |
| Muscle cramps, weakness, constipation | Hypokalemia associated with hyperaldosteronism |
| Delayed puberty | Congenital adrenal hyperplasia |
| Snoring | Sleep apnea |
| Prescription, over-the-counter, or illicit drug use | Drug-induced HTN |
| Medical History | |
| Umbilical artery catheterization | Renal artery thrombosis/renal embolus |
| Previous urinary tract infections | Renal scarring |
| Thyroid cancer, neurofibromatosis, von Hippel Lindau disease | Pheochromocytoma |
| Family History | |
| HTN | Inherited forms of HTN (AME, Gordon syndrome, Liddle syndrome, GRA), essential HTN |
| Renal disease | Polycystic kidney disease, Alport syndrome |
| Tumors | Familial pheochromocytoma, multiple endocrine neoplasia type II |
| Physical Examination Findings | |
| Vital Signs | |
| Tachycardia | Hyperthyroidism, pheochromocytoma, neuroblastoma, primary HTN |
| Bradycardia | Increased ICP (tumor, hydrocephalus) |
| Drop in BP from upper to lower extremities | Coarctation of aorta |
| General | |
| Growth retardation | Chronic kidney disease |
| Truncal obesity | Cushing disease, insulin resistance |
| Head and Neck | |
| Moon facies | Cushing disease |
| Elfin facies | Williams syndrome |
| Proptosis/goiter | Hyperthyroidism |
| Web neck | Turner syndrome |
| Adenotonsillar hypertrophy | Sleep disorders |
| Fundal changes | Chronic or severe HTN |
| Cardiovascular | |
| Friction rub | Systemic lupus erythematosus, collagen vascular disease, uremia |
| Apical heave | Left ventricular hypertrophy |
| Disparity in pulses | Coarctation |
| Lungs | |
| Crackles/rales | Heart failure |
| Abdomen | |
| Masses | Obstructive nephropathy, Wilms tumor, neuroblastoma, pheochromocytoma, polycystic kidney disease |
| Hepatomegaly | Heart failure |
| Bruit | Renal artery stenosis, abdominal coarctation |
| Genitalia | |
| Ambiguous, virilized | Congenital adrenal hyperplasia |
| Extremities | |
| Edema | Underlying kidney disease |
| Joint swelling | Autoimmune disease |
| Rickettsial changes | Chronic kidney disease |
| Dermatologic | |
| Neurofibromas | Neurofibromatosis |
| Tubers, ash leaf spots, adenoma sebaceum | Tuberous sclerosis |
| Bronzed skin | Excessive adrenocorticotropic hormone |
| Acanthosis nigricans | Insulin resistance/metabolic syndrome |
| Striae, acne | Cushing disease |
| Rashes | Vasculitis/nephritis |
| Needle tracks | Drug-induced HTN |
| Neurologic | |
| Mental status changes | Severe HTN |
| Cranial nerve palsy | Severe HTN |
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