Acute kidney injury (AKI); Renal colic; Hypertensive crisis.

There are more than 35 definitions of AKI (formerly acute renal failure) in literature!

Sudden interruption of kidney function resulting from obstruction, reduced circulation, or disease of the renal tissue;

Results in retention of toxins, fluids, and end products of metabolism;

Usually reversible with medical treatment; May progress to end stage renal disease, uremic

syndrome, and death without treatment.

Stage Increase in Serum Creatinine

Urine Output

1 1.5-2 times baseline OR 0.3 mg/dl increase from baseline

<0.5 ml/kg/h for >6 h

2 2-3 times baseline <0.5 ml/kg/h for >12 h

3 3 times baseline OR0.5 mg/dl increase if baseline>4mg/dlORAny RRT given

<0.3 ml/kg/h for >24 hOR Anuria for >12 h

Increase in SCr Urine output

Risk of renal injury

Injury to the kidney

Failure of kidney function

0.3 mg/dl increase

2 X baseline

3 X baseline OR

> 0.5 mg/dl increase if SCr >=4 mg/dl

< 0.5 ml/kg/hr for > 6 h

< 0.5 ml/kg/hr for >12h

Anuria for >12 h

Loss of kidney function

End-stage disease

Persistent renal failure for > 4 weeks

Persistent renal failure for > 3 months

Am J Kidney Dis. 2005 Dec;46(6):1038-48

AKI occurs in ≈ 7% of hospitalized patients. 36–67% of critically ill patients

(depending on the definition). 5-6% of intensive care unite (ICU)

patients with AKI require renal replacement therapy (RRP).

Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. American Journal of Kidney Diseases 2002; 39:930-936.

Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73.

Osterman M, Chang R: Acute Kidney Injury in the Intensive Care Unit according to RIFLE. Critical Care Medicine 2007; 35:1837-1843.

Mortality increases proportionately with increasing severity of AKI (using RIFLE).AKI requiring RRT is an independent risk factor for in-hospital mortality.Mortality in pts with AKI requiring RRT 50-70%.Even small changes in serum creatinine are associated with increased mortality.

Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital

mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73.

Chertow G, Levy E, Hammermeister K, et al.: Independent association between acute renal failure and mortality following cardiac surgery. American Journal of Medicine 1998; 104:343-348.

Uchino S, Kellum J, Bellomo R, et al.: Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA 2005; 294:813-818.

Coca S, Peixoto A, Garg A, et al.: The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. American Journal of Kidney Diseases 2007; 50:712-720.

.

Inhibition of tubular creatinine secretionTrimethoprim, Cimetidine, Probenecid

Interference with creatinine assays in the lab (false elevation) acetoacetate, ascorbic acid, cefoxitinflucytosine

Increased productionGl BleedingCatabolic states (Prolonged ICU stay)CorticosteroidsProtein loads (Total parenteral nutrition -Albumin infusion)

Persons at Risks◦Major surgery;◦Major trauma;◦Receiving nephrotoxic medications;◦Elderly.

Disease Category Incidence

Prerenal azotemia caused by acute renal hypoperfusion

55-60%

Intrinsic renal azotemia caused by acute diseases of renal parenchyma: -Large renal vessels dis.

-Small renal vessels and glomerular dis.

-Acute tubular necrosis (ATN) (ischemic and toxic)

-Tubulo-interestitial dis.

-Intratubular obstruction

35-40%

*>90%*

Postrenal azotemia caused by acute obstruction of the urinary tract

<5%

Intravascular volume depletionbleeding, GI loss, Renal loss, Skin loss, Third space loss

Decreased cardiac outputchronic heart failure (CHF)

Renal vasoconstrictionLiver Disease, Sepsis, Hypercalcemia

Pharmacologic impairment of autoregulation and GFR in specific settingsACEi in bilateral renal artery stenosis, nonsteroidal anti-inflammatory drugs (NSAIDs) in any renal hypoperfusion setting

Large Renal Vessel DiseaseThrombo-embolic disease

Renal Microvasculature and Glomerular DiseaseInflammatory: glomerulonephritis, allograft rejectionVasospastic: malignant hypertension, scleroderma crisis, pre-eclampsia, contrastHematologic: Hemolytic-Uremic Syndrome (HUS) & Thrombocytopenic Purpura (TTP), Disseminated intravascular coagulation

ATNIschemicToxic

Tubulo-interestitial DiseaseAcute Interestitial Nephritis (AIN), Acute cellular allograft rejection, viral (HIV, BK virus), infiltration (sarcoid)

Intratubular Obstructionmyoglobin, hemoglobin, myeloma light chains, uric acid, tumor lysis, drugs (indinavir, acyclovir, foscarnet, oxalate in ethylene glycol toxicity)

Stones; Blood clots; Papillary necrotic tissue; Urethral disease;

anatomic: posterior valvefunctional: anticholinergics, L-DOPA

Prostate disease; Bladder disease;

anatomic: cancer, schistosomiasisfunctional: neurogenic bladder.

Stages Onset – 1-3 days with ^ BUN and creatinine

and possible decreased urinary output (UOP); Oliguric – UOP < 400/d, ^BUN, Crest, Phos, K,

may last up to 14 d Diuretic – UOP ^ to as much as 4000 mL/d but

no waste products, at end of this stage may begin to see improvement

Recovery – things go back to normal or may remain insufficient and become chronic

History and Physical exam Detailed review of the chart, drugs administered,

procedures done, hemodynamics during the procedures.

Urinalysis protein, blood, crystals, infection

Urine microscopy casts, cells (eosinophils)

Urine lytes Renal imaging

Ultrasound, Mag-3 scan, Retrograde Pyelogram Markers of CKD

iPTH, size<9cm, anemia, high phosphate, low bicarb

Renal biopsy

1) Obtain a thorough history and physical; review the chart in detail;

2) Do everything you can to accurately assess volume status;

3) Always order a renal ultrasound; 4) Look at the urine;5) Review urinary indices.

Recognition of underlying risk factors◦ Diabetes◦ CKD◦ Age ◦ Hypertension (HTN)◦ Cardiac/liver dysfunction

Maintenance of renal perfusion Avoidance of hyperglycemia Avoidance of nephrotoxins

Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:261-275.

Subjective symptoms◦ Nausea◦ Loss of appetite;◦ Headache;◦ Lethargy;◦ Tingling in extremities.

Objective symptoms◦ Oliguric phase –

vomiting disorientation, edema, ^K+ decrease Na ^ BUN and

creatinine Acidosis uremic breath

•CHF and pulmonary edema•hypertension caused by hypovolemia, anorexia

•sudden drop in UOP•convulsions, coma•changes in bowels

Objective systoms◦ Diuretic phase

Increased UOP Gradual decline in BUN and creatinine Hypokalemia Hyponatriuemia Tachycardia

Diagnostic tests◦ Histoty&Physical (examenation)◦ BUN, creatinine, sodium, potassium. pH, bicarb.

Hgb and Hct◦ Urine studies◦ Ultrasound of kidneys◦ Kidneys, ureters, and bladder (KUB)◦ Abdomen and renal CT◦ Retrograde pyelogram

Avoid use of intravenous contrast in high risk patients if at all possible.

Use pre-procedure volume expansion using isotonic saline (?bicarbonate).

N-Acetylcysteine Avoid concomitant use of nephrotoxic

medications if possible. Use low volume low- or iso-osmolar contrast

Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:261-275.

Intravenous albumin significantly reduces the incidence of AKI and mortality in patients with cirrhosis.

Albumin decreases the incidence of AKI after large volume paracentesis.

Albumin and terlipressin decrease mortality in HRS.Sort P, Navasa M, Arroyo V, et al.: Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. New England Journal of Medicine 1999; 341:403-409.

Gines P, Tito L, Arroyo V, et al.: Randomised comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis. Gastroenterology 1988; 94:1493-1502.

Gluud L, Kjaer M, Christensen E: Terlipressin for hepatorenal syndrome. Cochrane Database Systematic Reviews 2006; CD005162.

Treatment is largely supportive in nature maintain renal perfusion

Correct metabolic derangements Provide adequate nutrition ? Role of diuretics RRT remains the cornerstone of

management of minority of patients with severe AKI

Human kidney has a compromised ability to autoregulate in AKI.

Maintaining haemodynamic stability and avoiding volume depletion are a priority in AKI.

Kelleher S, Robinette J, Conger J: Sympathetic nervous system in the loss of autoregulation in

acute renal failure. American Journal of Physiology 1984; 246: F379-386.

The individual BP target depends on age, co-morbidities (HTN) and the current acute illness.

A generally accepted target remains MAP ≥ 65.

Bourgoin A, Leone M, Delmas A, et al.: Increasing mean arterial pressure in patients with septic shock: Effects on oxygen variables and renal function. Critical Care Medicine 2005; 33:780-786

no statistical difference between volume resuscitation with saline or albumin in survival rates or need for RRT.

Finfer S, Bellomo R, Boyce N, et al.: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. New England Journal of Medicine 2004; 350: 2247-2256.

Fluid conservative therapy decreased ventilator days and didn’t increase the need for RRT in Acute Respiratory Distress Syndrome patients.

Association between positive fluid balance and increased mortality in AKI patients.

Wiedeman H, Wheeler A, Bernard G, et al.: Comparison of two fluid management strategies in acute lung injury. New England Journal of Medicine 2006; 354:2564-2575.

Payen D, de Pont A, Sakr Y, et al.; A positive fluid balance is associated with worse outcome in patients with acute renal failure. Critical Care 2008; 12: R74

There is no evidence that from a renal protection standpoint, there is a vasopressor agent of choice to improve kidney outcome.

Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the

Intensivist. Critical Care Medicine 2010; 38:261-275.

renal dose dopamine (<5 μg/kg of body weight/min) increases renal blood flow and, to a lesser extent, GFR. Dopamine is unable to prevent or alter the course of ischaemic or nephrotoxic AKI). Furthermore, dopamine, even at low doses, can induce tachy-arrhythmia’s, myocardial ischaemia, and extravasation out of the vein can cause severe necrosis. Thus, the routine administration of dopamine to patients for the prevention of AKI or incipient AKI is no longer justified.

Lauschke A, Teichgraber U, Frei U, et al.: “Low-dose” dopamine worsens renal perfusion in patients with acute renal failure. Kidney 2006; 69:1669-1674.Argalious M, Motta P, Khandwala F, et al.: “Renal dose” dopamine is associated with the risk of new onset atrial fibrillation after cardiac surgery. Critical Care Medicine 2005; 33:1327-1332.

Dopamine-1 receptor agonist, lack of Dopamine-2, and alpha-1 receptor effect, make it a potentially safer drug than Dopamine!

Reduces in hospital mortality and the need for RRT in AKI

Reverses renal hypoperfusion more effectively than renal dose Dopamine

So far so good specially in cardiothoracic ICU patients, awaiting more powered trials in other groups!

J Cardiothorac Vasc Anesth. 2008 Feb;22(1):23-6. J Cardiothorac Vasc Anesth. 2007 Dec;21(6):847-50Am J Kidney Dis. 2007 Jan;40(1):56-68Crit Care Med. 2006 Mar;34(3):707-14

Loop diuretics may convert an oliguric into a non-oliguric form of AKI that may allow easier fluid and/or nutritional support of the patient. Volume overload in AKI patients is common and diuretics may provide symptomatic benefit in that situation. However, loop diuretics are neither associated with improved survival, nor with better recovery of renal function in AKI.

JAMA. 2002 Nov 27;288(20):2547-53Crit Care Resusc. 2007 Mar;9(1):60-8

The most recent trials seem to confirm a potential positive preventive effect of N-acetylcysteine (NAC), particularly in contrast-induced nephropathy (CIN), NAC alone should never take the place of IV hydration in patients at risk for CIN; fluids likely have a more substantiated benefit. (150 mg/kg in 500 mL saline (0.9%)] over 30 min immediately before contrast exposure and followed by 50 mg/kg in 500 mL saline (0.9%) over the subsequent 4 h )

Erythropoietin (EPO) has tissue-protective effects and prevents tissue damage during ischaemia and inflammation, and currently trials are performed with EPO in the prevention of AKI post-cardiac surgery, CIN and post-kidney transplantation.

Nursing interventions◦ Monitor input/output,

including all body fluids◦ Monitor lab results◦ Watch hyperkalemia

symptoms: malaise, anorexia, parenthesia, or muscle weakness, EKG changes

◦ watch for hyperglycemia or hypoglycemia if receiving total parenteral nutrition or insulin infusions

•Maintain nutrition•Safety measures•Mouth care•Daily weights•Assess for signs of heart failure•Skin integrity problems•The nurse questions orders for potentially nephrotoxic drags, and the ordered dose is validated before the client receives the drag.

The primary nursing diagnosis and collaborative problems for the client with acute renal failure are Excess Fluid Volume, Potential for Pulmonary Edema, and Potential for Electrolyte Imbalances.

Nursing interventions:◦ Assess the client for early signs of pulmonary

edema.◦ Monitor serum electrolyte levels, vital signs,

oxygen saturation levels, hypertension.

26 yo F is involved in a motor vehicle accident , with multiple fractures, blunt chest and abdominal trauma. She was briefly hypotensive on arrival to emergency department, received 6L normal saline and normalized BP. Non contrast CT showed small retroperitoneal hematoma. On day#2 her SCr is 0.9 mg/dl, lipase is elevated and tense abdominal distension is noted. Ultrasound showed massive ascites. UOP drops to <20 cc/hr despite of 10 L total IV intake. On day#3, SCr is 2.1mg/dl, CVP is 17, UNa is 10 meq/L, with a bland sediment.

What is the cause of her AKI?What bedside diagnostic test and therapeutic

intervention is indicated?

Bladder pressure was 29 mmHg

UOP and SCr improved with emergent paracenthesis.

Dx: Abdominal Compartment Syndrome causing decreased renal perfusion from increased renal vein pressure.

59 yo M, s/p liver transplant in 2001 and acute on chronic rejection, now decompensated End Stage Liver Disease, is admitted with worsening ascites, hepatic encephalopathy and GI bleed (which is now controlled). The only medications he has been receiving are Lactulose and omeprazole. He has been hemodynamically stable with average BP~100/70 mmHg.He had a 3.5 L paracenthesis on day 2. His SCr has been slowly rising from 1.2 to 4.7 mg/dl within the 2nd to 4th day of admission and his UOP has dropped to 150 cc/day. His daily fractional excretion of sodium (FeNa) is <1% despite of 2 L fluid challenge. His Urine sediment is blend. His renal ulyrasound is normal.

What is the cause of his AKI?

Patient required hemodialysis (HD).

He had a second liver transplant and came off HD after the surgery with stable SCr of 1.4 mg/dl.

Dx: Hepatorenal Syndrome (HRS)

Major diagnostic criteria: No improvement with at least 1.5 L fluid

challengeSCr >1.5 mg/dl or GFR< 40 cc/minAbsence of proteinuria (<500 mg/d)Other causes are rouled out (obstruction,

ATN, etc.)Minor diagnostic criteria:

Urine volume < 400 cc/dayUNa < 10 meq/LSNa < 130 meq/LUrine RBC < 50/hpf

45 yo M with CHF and Bipolar Disorder on Lithium for 10 years, admitted for abdominal pain after a heavy meal, which turned out to be due to acute cholecyctitis. He was kept nil per os on D5 ½ normal saline 50 cc/hr. Next morning he felt well but thirsty and hungry, BP=120/80, input/output=1200/4500. His SCr rose from 1.2 to 1.9 mg/dl. SNa 149 meq/L. UNa 10 meq/L. UOsm 190 mOsm/Kg.

What is the cause of his AKI?

Patients intravenous fluids was changed to ½ normal saline, replacing 80% of UOP per hour. SCr and SNa improved to baseline in 2 days.

Dx: Prerenal azotemia secondary to renal free water loss in DI.

Medical treatment◦Hemodialysis Yugular, subclavian approach Femoral approach

◦Peritoneal dialysis◦Continous renal replacement therapy

(CRRT) Can be done continuously Does not require dialysate

Still evolving….Generally accepted◦ Oliguria/Anuria◦ Hyperammonemia◦ Hyperkalemia◦ Severe acidemia◦ Severe azotemia◦ Pulmonary Edema◦ Uremic complications◦ Severe electrolyte abnormalities◦ Drug overdose with a filterable toxin◦ Anasarca◦ Rhabdomyolysis

Client selection Dialysis settings Works using

passive transfer of toxins by diffusion

Anticoagulation needed, usually heparin treatment

HD catheter, dual or triple lumen, or arteriovenous shunt for temporary access

Advantages Maximum solute

clearance of 3 modalities

Best therapy for severe hyperkalemia

Limited anti-coagulation time

Bedside vascular access can be used

Disadvantages

•Hemodynamic instability•Hypoxemia•Rapid fluid and electrolyte shifts•Complex equipment•Specialized personnel•Difficult in small infants

Advantages Easy to use in ICU Rapid electrolyte

correction Excellent solute

clearances Rapid acid/base

correction Controllable fluid

balance Tolerated by unstable

patients Early use of total

parenteral nutrition Bedside vascular

access routine

Disadvantages•Systemic anticoagulation (except citrate)•Frequent filter clotting•Vascular access in infants

Postdialysis care:◦Monitor for complications such as

hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps.

◦Monitor vital signs and weight.◦Avoid invasive procedures 4 to 6 hours

after dialysis.◦Continually monitor for hemorrhage.

Solute and water transport via peritoneal membrane

Solute movement via diffusion + convection

Less problems of bio-incompatibility Loss of protein (10g/day) and middle

molecules

Advantages Simple to set up &

perform Easy to use in

infants Hemodynamic

stability No anti-coagulation Bedside peritoneal

access Treat severe

hypothermia or hyperthermia

Disadvantages•Unreliable ultrafiltration•Slow fluid & solute removal•Drainage failure & leakage•Catheter obstruction•Respiratory compromise•Hyperglycemia•Peritonitis•Not good for hyperammonemia or intoxication with dialyzable poisons

◦Glucose(13.6mg/ml, 22.7mg/ml, 38.6mg/ml)◦Sodium 132mmol/L◦Potassium 0mmol/L◦Calcium 1.25-1.75mmol/L◦Magnesium 0.25-0.75mmol/L◦Chloride 102mmol/L◦Lactate 35-40mmol/L◦pH 5.0-5.5

Subcutaneouscoupling

Externalsegment

of Tenckhoff catheter

External side of abdomen Abdominal cavity

Before treating, evaluate baseline vital signs, weight, and laboratory tests.

Continually monitor the client for respiratory distress, pain, and discomfort.

Monitor prescribed dwell time and initiate outflow.

Observe the outflow amount and pattern of fluid.

Protect vascular access

Monitor fluid balance indicators

Monitor IV carefully Assess for signs and

symptoms uremia Monitor

cardiopulmonary status carefully

Monitor BP

•Monitor medications•Address pain and discomfort•Infection control measures•Monitor dietary e-lytes and fluids•Skin care•CAPD catheter care if appropriate

The commonest urologic emergency One of the commonest causes of the

“Acute Abdomen” Sudden onset of severe pain in the flank Most often due to the passage of a stone

formed in the kidney, down through the ureter.

The pain is characteristically : ◦ very sudden onset◦ colicky in nature ◦ Radiates to the groin as the stone passes into the

lower ureter. ◦ May change in location, from the flank to the groin,

(the location of the pain does not provide a good indication of the position of the stone)

◦ The patient cannot get comfortable, and may roll around in agony.

◦ Associated with nausea/vomiting◦ the pain of a ureteric stone as being worse than the

pain of labour.

Differential diagnoses ◦ Leaking abdominal aortic aneurysms◦ Pneumonia◦ Myocardial infarction◦ Ovarian pathology (e.g., twisted ovarian cyst)◦ Acute appendicitis◦ Testicular torsion◦ Inflammatory bowel disease (Crohn’s, ulcerative

colitis)◦ Diverticulitis◦ Ectopic pregnancy ◦ Burst peptic ulcer◦ Bowel obstruction

Work Up :◦History◦Examination: patient want to move

around, in an attempt to find a comfortable position.

◦ +/- Fever ◦Pregnancy test◦Midstream urine

◦ Radiological investigation : Kidneys, ureters and bladders/ Abdominal US intravenous pyelogram (IVP) (was) Helical CT

advantages over IVP: greater specificity (95%) and sensitivity (97%) for

diagnosing ureteric stones Can identify other, non-stone causes of flank pain. No need for contrast administration. Faster, taking just a few minutes the cost of CT is equivalent to that of IVP

Magnetic resonance imaging very accurate way of determining whether or not a

stone is present in the ureter very high cost

Acute Management of Ureteric Stones:◦ Pain relief NSAIDs Intramuscular or intravenous injection, by

mouth, or per rectum +/- Opiate analgesics (pethidine or

morphine).◦? Hyperhydration◦ ‘watchful waiting’ with analgesic

supplements 95% of stones measuring 5mm or less pass

spontaneously

Indications for Intervention to Relieve Obstruction and/or Remove the Stone:◦Pain that fails to respond to analgesics.◦Associated fever.◦Renal function is impaired because of the

stone (solitary kidney obstructed by a stone, bilateral ureteric stones, or preexisting renal impairment )

◦ Obstruction unrelieved for >4 weeks ◦ Personal or occupational reasons

Treatment of the Stone:◦ Temporary relief of the obstruction: Insertion of a JJ stent or percutaneous

nephrostomy tube.◦Definitive treatment of a ureteric stone: Extracorporeal shock wave lithotripsy Percutaneous nephrolithotomy Ureteroscopy Open Surgery: very limited.

The nurse examines the client to detect bladder distention. The physical examination may reveal pale, ashen, diaphoretic skin; the client may suffer from excruciating pain. Vital signs may be moderately elevated with pain; body temperature and pulse are elevated with infection. Blood pressure may decrease markedly if the severe pain causes shock.

Nursing interventions are focused on pain management and prevention of infection and urinary obstruction.

The nurse administers the medication and assesses the response by asking the client to rate the discomfort on a rating scale.

The nurse strains the urine to monitor for excretion of the calculus. Any stones obtained are sent to the laboratory for analysis; preventive therapy is based on stone composition.

DefinitionsDefinitions

Hypertensive Emergency: A relatively high blood pressure with evidence of target organ damage. BP >180/120

Hypertensive Urgency: Elevated BP with imminent risk of target organ damage

DefinitionsDefinitions

Acute Hypertensive Episode: SBP >180 or DBP >110 and no target organ damage

Transient Hypertension: Hypertension that occurs in association with

•pain •withdrawal syndromes•some toxic substances•anxiety•cessation of medications

PathophysiologyPathophysiology

•Poorly understood•Varies with etiology•Rate of rise: Important in pathology•There is a sudden increase in systemic vascular resistance and circulating humoral vasoconstrictors•Loss of an organ’s auto-regulation capability occurs

Target organ dysfunction

What’s ImportantWhat’s Important??

•Not the degree of BP elevation but•The clinical status of the patient that defines an emergency.•BP alone does not determine an emergency.•The degree of target organ involvement that determines the rapidity with which the BP should be lowered.

TypesTypes

•Aortic dissection•Pulmonary edema•MI•Acute coronary syndrome •Acute renal failure•HELLP syndrome•Severe pre-eclampsia•Eclampsia

•Hypertensive encephalopathy•Subarachnoid hemorrhage•Intracranial hemorrhage•Acute ischemic stroke•Sympathetic crisis

Target Organ Damage Associated with Target Organ Damage Associated with Hypertensive EmergenciesHypertensive Emergencies

•Cerebral infarction: 24.5% of cases•Hypertensive encephalopathy: 16.3%•Acute decompensated heart failure: 14.3%•Acute coronary syndrome: 12.0%•ICH: 4.5%•Aortic dissection: 2.0%

General Management Goals

•Reduce BP so autoregulation can be re-established •Typically, this is a ~25% reduction in MAP•Or, reduce MAP to 110-115•Avoid

- Lowering the BP too much or too fast. - Treating non-emergent hypertension

General Management Goals

•Exceptions: aortic dissection and eclampsia

•In aortic dissection and eclampsia, BP should be lowered to normal levels

•Search for secondary causes

Risk of Rapid BP ReductionRisk of Rapid BP Reduction

•Acute renal deterioration•Ischemic cardiac event•Ischemic cerebral event•Retinal artery occlusion (blindness)

LabetalolLabetalol

•β-blocker & weak α-1 effects•Without reflex tachycardia

•Commonly used•Broad applications

•Exceptions•Cocaine intoxication•Decompensated heart failure

•Bolus: 10-20mg IV over 2 min.•40-80 mg & 10-min intervals up to 300 mg total.•Check BP 5 & 10 min. after bolus

•Infusion: 2mg/min and titrate to response up to 300 mg.•Effect: 2-5 min.; peaks @ 15 min and lasts 2-4 hours.•Avoid in

•Bradycardia, heart block, bronchospasm, CHF.

EsmololEsmolol•Ultra-short, cardioselective β-blocker.

- β1 receptors chiefly in cardiac muscle - Higher doses: β2 receptors in bronchi and vascular muscle elsewhere

•Loading dose: 250-500mcg/kg IV over 1-3 min. then•Infusion: 50 mcg/kg/min over 4 min. •May repeat loading dose and increase infusion rate in increments of 50 mcg/kg/min up to 4 times. -Effect: Within 60 sec.; lasts 10-20 minutes.

•½-life: 8 min.•Avoid in

- Bradycardia, heart block, bronchospasm, CHF.

NicardipineNicardipine•2nd-generation calcium channel blocker (inhibits influx of Ca ions into cardiac/vascular smooth muscle)

- Selective for cerebral and coronary arteries - Dose-dependent decrease in systemic vascular resistance

•Continuous infusion: 5mg/hr - May increase by 2.5 mg/hr q 15 min. until target pressure or dose of 15 mg/hr is reached.

•Onset: 5-10 min.•Duration: 1-4 hours. - Safe in neurologic hypertensive emergencies

•Doesn’t increase ICP•Favorable effect on myocardial oxygen balance•Avoid with IV β-blockers•Caution in CHF, aortic stenosis.

NitroglycerinNitroglycerin•Venodilator

- Arteriodilator at high doses•Reduces preload, cardiac outpute, cardiac workload

- First-line in CHF & CAS•Continuous infusion

- 5 mcg/min, increase by 5 q 3-5 min up to 20 mcg/min - Then by 10 mcg/min q 3-5 min. up to 200 mcg/min.

•Onset: 2 min.•Duration: 1 hour•Avoid: Renal/cerebral hypoperfusion, Viagra.

NitroprussideNitroprusside•Arterio- & Venodilator

- Decreases preload & afterload - Potential, as a general vasodilator, to increase ICP

•Continuous infusion - 0.3-0.5 mcg/kg/min, increase by 0.5 mcg/kg/min and titrate.

•Onset: Seconds•Duration: 1-2 minutes•Caution: >2 mcg/kg/min may lead to CN toxicity•Avoid: Renal/hepatic failure, neurovascular emergencies, increased ICP.•Recommended when all else fails.

- May be added to other anti-hypertensives

PhentolaminePhentolamine•α-1 & α-2 blocker•Bolus

- 5-20 mg IV q 5 min.•Infusion

- 0.2-0.5 mg/min•Indications

- Cocaine intoxication - Pheochromocytoma

•May induce - MI - Cerebral vascular accident

FenoldopamFenoldopam•Dopamine-1 agonist•Infusion: 0.1 mcg/kg/min and titrate q 15 min.

- Range: 0.1 – 1.6 mcg/kg/min•Onset: 5 min.•Peak: 15 min.•Duration: 30-60 min.•Improves Cr clearance & urine flow•Applications

- Renal/neurologic hypertensive emergencies•S.E.: Flushing, dizziness, vomiting

EnalaprilatEnalaprilat•ACE inhibitor

- Only 1 IV•Application

- CHF - Acute CAS

•Test dose: 0.625 mg - Hypotension common with 1st dose

•Bolus: 1.25 mg over 5 min q 4-6 h•Onset: Within 15 min.•Maximum effect: 1-4 hours•Avoid in pregnancy, angioedema

Pathophysiology: Pathophysiology: •Loss of Cerebral Autoregulation of blood flow resulting in hyperperfusion of the brain, loss of integrity of the blood brain barrier, and vascular necrosis. •Loss of Autoregulation occurs at a constant cerebral blood flow of above MAP 150 to 160 mmHg. •Acute Onset•Reversible

SymptomsSymptoms: Headache, Nausea/Vomiting, Lethargy, Confusion, Lateralizing neurological symptoms that are not often in an anatomical distribution.

SignsSigns: Papilledema, Retinal Hemorrhages Decreased level of consciousness, Coma Focal neurological findings

Clinical manifestation of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation

Defined as an acute organic brain syndrome or delirium in the setting of severe hypertension

Not adequately treated – cerebral heamorrhage, coma and death.

BUT with proper treatment – completely reversible

Clinical diagnoses (exclusion)

Management

Reduce MAP by 20 to 25% and do not exceed this within first 30 to 60 min.

Rosen recommends reduction of 30 to 40% Treatment Reduces vasospasm that occurs at these

high pressures Avoid excessive BP reduction to prevent

hypoperfusion of the brain and further cerebral ischemia

TherapyTherapy

Nitroprusside◦ 1st line, 0.3 – 10 mcg/kg/minute

Labetalol Enalaprilat Fenoldopam

PathophysiologyPathophysiology

Abrupt, severe increase in afterload leads to systolic and diastolic dysfunction.

Vicious cycle ensues:◦ Heart failure causes poor coronary perfusion, LV

ischemia and worsening failure◦ CHF leads to hypoxia and worsens LV ischemia◦ Renal hypoperfusion leads to renin release and this

increases afterload

Signs and SymptomsSigns and Symptoms

Abrupt and severe dyspnea, tachypnea, and diaphoresis

Rales, wheezes, distant breath sounds, frothy sputum, and gallop rhythm

Goals of therapyGoals of therapy

Reduce preload and afterload! Minimize coronary ischemia by increasing supply

(blood to coronary arteries) and decrease demand (wall tension, tachycardia)

Oxygenate, ventilate, clear pulmonary edema.

TherapyTherapy

Nitroglycerin◦ Arterial (especially coronaries) and venodilator,

reducing preload and afterload Lasix

◦ Initially a vasodilator, then diuretic Morphine

◦ Vasodilator and sympatholytic ACE inhibitor

◦ Interrupts the renin-angiotensin-aldosterone axis

TherapyTherapy

Definitive therapy is delivery of the fetus and placenta

Magnesium: 4-6gm over 15 minutes, drip 1-2gm per hour

Hydralazine: 5-10mg IV, drip 5-10mg per hour Labetalol: 20mg IV, repeat prn q 10 minutes, drip

1-2mg per minute