VIEWS: 0 PAGES: 72 POSTED ON: 7/18/2013
Dr. Mahesh A. Mohite Sai Child Care Clinic New Panvel, Maharashtra 8 yrs male Admitted for seizure. Went to school at 9 am, had uneasy feeling with lethargy and later giddiness so parents were called to school. Mother took him to nearby nursing home, and on way child convulsed (11am). Admitted : seizure stopped immediately with lorazepam. History suggested focal seizure--CT brain --reported small lipomeningeal cyst --put on oxcarbazine. Was HD stable for next 18 hrs, but not alert still, so review detail examination -- revealed hypertension. BP was 160/140mmhg. Referred to tertiary care: ◦ Pappiloedem present. ◦ Detail evaluation revealed left kidney contracted with clot in aorta and at the origin of left renal artery. ◦ Child had intractable HT not responding to medications and succumbed to HT encephalopathy. HT in children is common (1-4%); but it is clinically silent till it becomes severe so routine BP recording is must. 1 1. Every child above 3 yrs age BP should be recorded atleast once a year (WHO). Every child on admission– BP should be recorded. Once HT is confirmed it is important to rule out HT as protective body response. ◦ 8 yrs male ◦ Brought with c/o --pain in hips, inability to walk ◦ h/o pneumonia- 15 days ago- treated by GP with antibiotics and steroids ? ◦ Confirmed resolution of x-ray picture after 8 days. ◦ O/E: HR 140/min, BP 140/96mm, lethargic, RR-36/min, CRT 4 sec tense abdomen gaseous, passing urine regularly ◦ Investigations: Cxr- lt lobar pneumonia, CBC- 30000/74/24, plat-5.74lac SGPT- 1335 iu, PT/PTT INR 1.8, S. creat-0.7 ◦ Monitored in PICU ◦ Convulsed 2 times in first 3 hrs of admission. ◦ Nasal bleed local, packed by ENT surgeon. ◦ Rapid desaturation– shock progressed rapidly-- succumbs within 24 hrs of admission Where we lost him? ◦ HYPERTENSION MISLEAD US. ◦ Valuable time lost. ◦ Hypertension can be compensatory response to shock and other signs of shock has to be looked for. 5 yrs/F Admitted with 10 days fever, lethargy since 3 days, H/o rash on body on D3 to 5 of fever Lepto epidemic period Investigations reveled CBC not significant, lepto IgM +ve, CSF: 48 cells, 80% lympho, sugar-48 (92), prot-52 Was being treated as lepto immune encephalitis. Progressive lethargy on D2 of admission Jr. consultant on night duty noticed BP 136/98 Gave amlodipin 0.1 mg/kg Child deteriorated became comatose, decerebrte Cerebral immaging revealed hydrocephalus with raised ICP. Conclusion: It was TBM with hydrocephalus with progressive raised ICP HT was part of cushing triad, a protective response to maintain cerebral perfusion. Ideal treatment was to decrease ICP and not antihypertensive. 2 In emergency scenario with critical HT ◦ Rule out protective HT Hypertensive shock Hypertension secondary to raised ICP ◦ then ◦ Categorize the HT which will decide how aggressively treatment is needed. What is Hypertensive (HT) emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? What is HT emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? Blood pressure-wise categories (2004 revised): ◦ Parameters set according to blood pressure for age, sex and height – percentiles: Normal range: <90th percentile Pre-hypertensive or high normal (JNC7): 90-95th percentile– high BMI adolescents. Hypertension: Class I: >95th PC----<99th PC+5mmhg Class II: >99th percentile + 5 mm hg Making it simple: ◦ Systolic BP > 100+ age (yrs) X 2 mm Hg. e.g. Categorization based on presenting clinical syndromes: Hypertensive URGENCY: critical hypertensive presentation with imminent risk of target organ damage. Hypertensive EMERGENCY: critical hypertensive presentation with evidence of established target organ damage. Accelerated Hypertension: BP is elevated progressively, at fast pace, with retinal hemorrhage and exudates (Grade III Keith-Wagner-Barker retinopathy ). Malignant hypertension: hypertensive emergency with papilloedema, retinal hemorrhage (Grade IV Keith-Wagner- Barker retinopathy.) 3 Screen for Target organs: ◦ Neuronal: Encephalopathy Intracranial hemorrhage Acute stroke ◦ Cardio-vascular: Acute myocardial ischemia LVF/CCF Dissection of aorta ◦ Renal: Acute renal failure. Microangiopathic hemolytic anemia. ◦ Retinal Papilloedema, Retinal hemorrhage Secondary HT: Renal : most common cause in ped age Parenchymal – glomerular (salt and water retension); non- glomerular (R-A- A) Renovascular –(increased R-A-A axis) Endocrinal: Renin secreting tumors– (increased renin) Pheochromocytomas, neuroblastoma –( increased catecholamines) Cushing—(increased aldosterone) Hyperthyroid—(increased catecholamines) Coarctation of aorta—(increased R-A-A axis) Drugs and toxins- cocaine, cyclosporin, tachrolimus, steroids Essntial or idopathic or primary HT ◦ Infant: Congenital renal diseases, reno-vasular, renal parenchymal, co- arctation of aorta. ◦ Toddler: Reno-vascular, reno parenchymal, reflux nephropathy, co- arctation of aorta. ◦ School going child: AGN most common ◦ Second decade and adolescent: essential HT ◦ Endocrinal HT : present at all ages. Flushing, tachycardia, mood changes, wt loss, Ht. discripancies. All these s/s are difficult to appreciate in infant so common clinical pick up at later ages, and early age children picked up on investigations. At this stage it is clear that: ◦ Essential HT rarely causes HT emergency ◦ 4 Commonest cause of HT emergency in children less than 10 yrs is renal (90%)– either congenital, parenchymal or reno-vascular. 2008 Mar-Apr;31(2):153-8. Clinical experience of childhood hypertensive encephalopathy over an eight year period. Hu MH, Wang HS, Lin KL, Huang JL, Hsia SH, Chou ML, Hung PC, Hsieh MY, Wong AM. Source Division of Pediatric Critical Care and Emergency Medicine, Chang Gung Children's Hospital, Taipei, Taiwan, R.O.C. Abstract BACKGROUND: Hypertensive encephalopathy is an uncommon neurological syndrome in children, usually with reversible clinical and neuroimaging findings. Little is known about the precipitating factors, clinical presentations, neuroimaging findings and outcomes of childhood hypertensive encephalopathy in Taiwan. METHODS: To characterize this syndrome, we retrospectively analyzed 12 children with hypertensive encephalopathy in a tertiary institution from 1998 through 2005. We investigated the precipitating factors, clinical findings, courses, neuroimaging characteristics and outcomes. RESULTS: Twelve patients (10 boys and 2 girls) with hypertensive encephalopathy were identified. Post-streptococcal glomerulonephritis was the most common precipitating underlying disease. Common clinical presentations included mental change (100%), seizure (91.6%), headache (66.6%), nausea or vomiting (75%), and blurred vision (41.6%). Brain imaging studies showed vasogenic edema over the bilateral parietal, occipital and parasagittal regions, or the cerebellum. All patients had a reversible clinical course. CONCLUSION: Hypertensive encephalopathy is predominant in males, and mental change is the most common clinical presentation. Renal origin is a common precipitating factor. A characteristic lesion of hypertensive encephalopathy is occipitoparietal region edema. The overall clinical outcome is good after prompt treatment. 2010 Feb;51(1):44-51. Clinical analysis of hypertension in children admitted to the emergency department. Yang WC, Wu HP. Source Department of Pediatrics, Changhua Christian Hospital, Changhua, Taiwan. Abstract BACKGROUND: Hypertension in children is a relatively rare disease and has a high risk of further severe damage. The current study aimed to survey the clinical spectrum of hypertension in children admitted to an emergency department (ED). METHODS: We reviewed the medical records of all children aged 18 years and younger in whom a diagnosis of hypertension was made at the ED in Changhua Christian Hospital between 1998 and 2008. The patients were divided into four age groups (infants, preschool-age, school-age and adolescents) and three severity levels (transient hypertension, hypertension and hypertensive crisis). Case distribution analysis of hypertension based on different months and years was performed. Body mass index, blood pressure, etiologies and presenting symptoms were also analyzed according to age groups and severity levels. RESULTS: A total of 99 children met the inclusion criteria and were included in the current study. Diagnoses included 15 transient hypertension (15.1%), 28 hypertension (28.3%) and 56 hypertensive crises (56.6%). Almost all of the hypertensive crisis patients presented with stage 2 hypertension (n = 55, 98.2%). Dizziness and headache were the most common presenting symptom in patients in school-age and adolescent groups. Of the symptoms described, altered mental status and coma were most common in preschool-age and school-age groups. Neurologic disorder (26.3%) was the most common etiology in children younger than 6 years of age, followed by renal disorders (21.0%). In children older than 6 years of age, the major etiologies of hypertension and hypertensive crisis included untreated primary hypertension, renal disorders and endocrine disorders. CONCLUSION: Hypertension in children may be easily underestimated but is potentially life-threatening in the pediatric ED. Primary care clinicians should promptly identify patients with stage 2 hypertension and treat them immediately and appropriately to prevent damage to cardiovascular organs. 2007 Aug;34(3):316-21. Acute glomerulonephritis presenting with PRES: a report of 4 cases. Wirrell EC, Hamiwka LD, Hamiwka LA, Grisaru S, Wei X. Source Division of Pediatric Neurology, Department of Pediatrics and Clinical Neurosciences, University of Calgary, Calgary, AB, Canada. Abstract OBJECTIVE: Posterior reversible encephalopathy syndrome (PRES) occurs most commonly in the setting of known hypertension or use of immunosuppressive agents. DESIGN AND METHODS: We report four previously-well children who presented acutely with altered mentation, seizures and visual disturbances and were diagnosed with PRES. RESULTS: Only one child had a history of gross hematuria prior to the seizure. All four were discovered to be hypertensive only after onset of their neurological symptoms, and were subsequently diagnosed with glomerulonephritis. All four had rapid resolution of neurological symptoms with adequate treatment of hypertension. CONCLUSIONS: Blood pressure must be measured promptly in all children presenting with these symptoms. If elevated, the diagnosis of PRES should be strongly considered and a workup for renal disease pursued. Recognize iatrogenic or reactive HT and when necessary correct them: HT with tachycardia: Non-convulsive seizures (pupils, eye movements) Autonomic dysfunctions: GBS, polio Uncontrolled pain and agitation Withdrawal from narcotics and benzodiazepines Fluid overload Hypercapnea Drugs: aminophylline, β agonist, tacrolimus, steroids HT with bradycardia: Raised ICP Drugs: steroids Pressure effects: Brain: hemorrhages Heart: LVF Aorta: dissection Kidney: acute shut down, micro-angiopathic hemolysis. Retina: bleed, detachment etc. 5 Failed auto-regulation in target organs like brain, kidney, retina MAP-à ◦ Rate of elevation of BP is more important than level of BP. ◦ Level of BP at which emergency manifestations occur are variable in different patients. ◦ Chronic hypertensives have lesser chance of emergency situations vs newly detected hypertensives– vascular walls are modified for stress in chronic hypertensives and autoregulatory range gradually resets at higher levels. What is Ht emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? Features related to hypertension Features related to target organ injury. Features of underlying primary disease. Renal disease Endocrinal disease Drug history Features related to HT will be variable with age of presentation: Neonatal/infant HT: lethargy, irritability. Older child: headache, vomiting, dissiness, blurred vision, epistaxis. HT encephalopathy ◦ Presentation: Acute onset headache, nausea, vomiting, altered mental status, blurred vision, blindness, seizure, stroke, coma and death. ◦ Is HT cause or effect of raised ICP? 5 yrs/F Admitted with 10 days fever, lethargy since 3 days, H/o rash on body on D3 to 5 of fever Lepto epidemic period Investigations reveled lepto IgM +ve, CSF: 48 cells, 80% lympho, sugar-48 (92), prot-52 Was being treated as lepto immune encephalitis. Progressive lethargy on D2 of admission Jr. consultant on night duty noticed BP 136/98 Gave amlodipin 0.1 mg/kg Child deteriorated became comatose, decerebrte Cerebral immaging revealed hydrocephalus with raised ICP, basal exudates. Conclusion: It was TBM with hydrocephalus with progressive raised ICP HT was part of Cushing triad, a protective response to maintain cerebral perfusion. Ideal treatment was to decrease ICP and not antihypertensive. ◦ Is HT cause or effect of raised ICP? Usually BP (HT) levels needed to cause encephalopathy is very high. BP (HT) secondary to raised ICP is relatively low. HT sec to raised ICP usually resolves spontaneously in 48 hrs. History of onset and progress of disease will help in recognizing the primary cause. CCF ◦ Common presentation: dyspnea, tachypnea, orthopnea, cough, bronchospasm, hemoptesis, chest pain, abdominal pain ◦ Presentation as shock: Cardiogenic shock CCF is common presentation; --- 5 yrs male Referred for gasping respiration. O/E: pulseless child, gasping respiration, CRT 5 sec with cold ext, liver 5 cm. Admitted to PICU-- intubated– ventilated. O/E: pulses now palpable, but poor volume. Consultant orders to give fluid bolus and attempts to record BP. BP: 150/130mmgh With ventilatory management and pulmonary edema management child gradually settled and extubated. Investigations revealed urine casts, RBCs and C3 low– s/o AGN. In such presentation underlying pathology may be totally masked. 6 Cardiac failure presentation is more common in infants and early childhood. Neurological presentation is more common in later age groups. Dissection of aorta: Acute onset chest or abdominal pain depending upon site of dissection pulse deficit, sign of end-organ circulatory compromise– on the background of HT. Renal compromise: Acute Renal failure Microangiopathic hematuria What is Ht emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? Quick evaluation Is it the body’s protective mechanism? Control HT with appropriate medication: Investigate for extent of target organ injury and treat it. Investigate for primary cause and treat it. Wean on to long-term medications-- when ever needed— after 12-24 hrs of HT emergency control. ◦ CBC: HB, e/o hemolysis Anemia- chronic renal disease, HUS; Micro-angiopathic hemolysis– HUS, effect of HT on kidneys Thrombocytopenia– HUS ◦ Renal function: complete urine routine analysis, urine for casts, RBCs, WBCs, BUN, S. Creat ◦ Cardiac evaluation in CCF presentation: ECG, x-ray chest if possible echo to know chronicity and cardiac effects of HT; also important in co-arctation. ◦ CNS evaluation in neurological presentation: CT-scan brain to know I/C lesions. ◦ Further detail investigations to be done after HT is stabilized. Documented HT EMERGENT UL / LL BP difference (R-F delay) APPROACH Yes No Coarctation Abnormal of aorta urine analysis Yes No Predominant Predominant WBC RBC, albumin Plasma renin Reflux uropathy Glomeruler disease, AGN, Recurrent UTI SLE, HSP, nephrocalcinosis, Renal anomaly nephrolithiasis, renal vein thrombosis Low High Normal/high Endocrine- Renovascular Essential What is Ht emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? Whether urgency or emergency management principles remain same. Goals of management: Reduce BP to normal or near normal level (below 90th PC). Prevent target organ injury. Revert primary cause of HT whenever possible. ◦ Important principle: 7 Reduce BP by 25% of MAP in first 15 min to 2 hrs, next 25% in next 12 to 24 hrs and rest over 48 hrs-- avoid catastrophic fall. Exception is HT emergency with dissection of aorta where BP should be brought down very fast to normal levels. Keep saline bolus ready to counter catastrophic fall in BP. Monitoring: Invasive BP monitoring is highly desirable; if not possible manual BP measurement every 15 min is adviced. Monitor Clinically for sensorium, pupillary response and visual acuity. What is Ht emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? Ideal drug: Drug having rapid onset of action, Short half life (rapid offset of action) so Ease of titration. Iv drugs can provide these qualities and are the preferred ones for HT emergencies. Best drugs are smooth muscle relaxants causing vasodialatation. Commonly used drugs: Sodium nitroprusside* Labetolol* Nefedepin* Nitroglycerine* Fenoldopam Nicardipine Esmolol Sodium nitroprusside: Vasodialator-- arterial and venous– Advantage: Rapid onset and offset of action Disadvantage: Not ideal in HT encephalopathy– controversial- Meth-Hb and cyanide toxicity. Toxicity– unexplained met acidosis, incr. lactate, cellular hypoxia, tremors, vomiting, seizures etc.– unsafe for >24 hrs use Dose: 0.25mic/kg/min titrate up to 3mic/kg/min. Caution: cover the infusion with aluminum foil Labetolol: Combined β and α blocker. β seven times more potent. Advantage: Rapid onset 5-10 min, duration 3-6 hrs. Safe in HT encephalopathy. Useful in pheochromocytoma (α, β) both blocked Good drug in all HT emergencies Disadvantage: Contraindicated in CCF, asthma, chronic resp diseases Caution in diabetes– masks hypoglycemia. Hypokalemia, hypotension, nausea Dose: Bolus: 1-3 mg iv over 1hr Infusion: 0.25mg/kg/hr increased to 3mg/kg/hr 2011 Jan;12(1):28-32. Safety and efficacy of intravenous labetalol for hypertensive crisis in infants and small children. Thomas CA, Moffett BS, Wagner JL, Mott AR, Feig DI. Source Department of Pharmacy, Texas Children's Hospital, Houston, Texas, USA. firstname.lastname@example.org Abstract OBJECTIVE: To determine the efficacy and safety of labetalol for hypertensive crisis in children ≤ 24 months of age. Twenty-seven patients ≤ 24 months of age were treated with 37 intravenous infusions of labetalol, nicardipine, or nitroprusside for hypertensive crisis or hypertensive urgency. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The primary end point consisted of time to 20% reduction in systolic blood pressure. Primary safety end points measured the prevalence of deleterious effects of labetalol. Continuous infusion of labetalol reduced mean systolic blood pressure by at least 20% in < 8 hrs. This effect was similar to nicardipine and nitroprusside infusions. The reported side effects were similar in each group. Patients receiving labetalol and presenting with ischemic or traumatic brain injury were likely to develop hypotension requiring infusion discontinuation. CONCLUSIONS: Continuous intravenous labetalol infusion is efficacious for treatment of hypertensive crisis in children ≤ 24 months of age. Aside from patients presenting with ischemic or traumatic brain injury, labetalol was safe to use in this population for hypertensive emergencies and had a satisfactory adverse effect profile. Labetalol may reach dose saturation at a much lower dose in young children in comparison to adults. Clinicians should use caution when initiating labetalol infusions in young patients with brain injury. Nefidepin: Calcium channel blocker; vasodialator Advantage: Oral prep available– oral / SL same effect Acute onset HT urgency as in AGN it is very effective and safe. Slow steady onset 30min. Disadvantage: Unpredictable, rapid fall in BP in chronic HT can fail cerebral auto-regulation and lead to CNS damage (pediatric studies support it’s safety). Contraindicated in raised ICP and ICH Dose: 0.25-0.5 mg/kg 6-8 hrly; repeat sos after 30 min. Blaszak et al published a retrospective study of 117 children treated with nifedipine, determining that the drug is safe and effective provided the initial dose is no greater than 0.25 mg/kg. No clinically significant side effects were observed during the study. Nitroglycerine infusion: ◦ IV: 0.1 mic/kg/min titrate to 0.5 mic/kg/min ◦ Greater venodilation than arteriolar dilation ◦ Most useful in pts with evidence of myocardial injury and coronary insufficiency. ◦ Onset of action is 2-5 minutes ◦ Duration of action is 5-10 minutes ◦ Headache and tachycardia –side effects What is Ht emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? Hypertensive encephalopathy or sub-arachnoid hemorrhage: labetalol , iv nitroprusside (controversies) CHF with pulmonary edema: Iv nitroprusside, NTG, furosemide, morphine Acute aortic dissection: iv nitroprusside + b-blockers (esmolol), labetolol. Acute myocardial ischemia: iv NTG, b-blockers, ACE inhibitors. HT urgency Iv labetolol, NTG drip, nifedipine, amlodipin 8 Labetolol is safe and effective and may need lesser monitoring– Used in all HT emergencies except contraindications Sodium nitroprusside is immediate choice for all HT emergencies in children when used for less than 36 to 48 hrs; Used in all HT emergencies except myocardial injury and HT encephalopathy. NTG for ischemic myocardial injury What is Ht emergency? How it presents? What are priorities in such emergency? What are principles of management of HT emergency? What drugs are available? What is practical choice of drug in given situation? What about weaning and long-term management? When to start weaning ICU anti-HT? Acute effects of target organ damage are controlled– e.g. CCF, encephalopathy, signs of progressive stroke etc are controlled. Oral anti HT drugs are started 6-12 hrs after i.v. drugs and i.v. are slowly withdrawn as soon as initial targets are achieved. Increased salt and water retension: e.g. AGN Diuretics in addition to vasodialators Renin-angiotensin-aldosterone axis stimulation: e.g. renovascular disease, co-arctation of aorta ACE inhibitors in addition to vasodialators; B-blocker like propranolol may have added advantage. Excess catecholamines: e.g. pheocromocytoma, thyrotoxicosis α-blockers (phentolamine) followed by β-blockers Increased aldosterone: e.g. Cushings Spironolactone ◦ Cautions in certain situations: HT encephalopathy: be extra caucious with nitroprusside– vasodialatation increases blood flow to brain hence ICP. In pheocromocytoma initially give phenoxybenzamine (α- blocker) and later add β-blocker. ACE inhibitors to be avoided in bilateral reno-vascular HT. Record BP in every emergency/ every admission. Recognize hypertensive urgency end emergency. Rule out hypertension as a protective phenomena. Renal diseases contribute to 90% HT emergencies In HT emergencies bring down BP slowly. Labetolol and Sodium Nitroprusside are primary choice drugs. Avoid target organ injury. Recognize and treat the underlying cause.
Pages to are hidden for
"Hypertensive emergencies…"Please download to view full document