Docstoc

Hypertensive emergencies…

Document Sample
Hypertensive emergencies… Powered By Docstoc
					   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. cthoma15@clarian.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.

				
DOCUMENT INFO
Shared By:
Categories:
Tags:
Stats:
views:0
posted:7/18/2013
language:English
pages:72