Download 04. Acute Kidney Injury

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
OR
0.5 mg/dl increase if
baseline>4mg/dl
OR
Any RRT given
<0.3 ml/kg/h for >24
h
OR
Anuria for >12 h
Increase in SCr
Urine output
Risk of renal injury
0.3 mg/dl increase
< 0.5 ml/kg/hr for > 6 h
Injury to the kidney
2 X baseline
< 0.5 ml/kg/hr for >12h
Failure of kidney
function
3 X baseline OR
> 0.5 mg/dl increase if
SCr >=4 mg/dl
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 secretion
Trimethoprim, Cimetidine, Probenecid
Interference with creatinine assays in the
lab (false elevation)
acetoacetate, ascorbic acid, cefoxitin
flucytosine

Increased production
Gl Bleeding
Catabolic states (Prolonged ICU stay)
Corticosteroids
Protein loads (Total parenteral nutrition Albumin infusion)

Persons at Risks
◦ Major surgery;
◦ Major trauma;
◦ Receiving nephrotoxic medications;
◦ Elderly.
Disease Category
Prerenal azotemia caused by acute renal
hypoperfusion
Incidence
Intrinsic renal azotemia caused by acute
diseases of renal parenchyma:
35-40%
-Large renal vessels dis.
-Small renal vessels and glomerular dis.
-Acute tubular necrosis (ATN) (ischemic and toxic)
-Tubulo-interestitial dis.
-Intratubular obstruction
Postrenal azotemia caused by acute
obstruction of the urinary tract
55-60%
*>90%*
<5%

Intravascular volume depletion
bleeding, GI loss, Renal loss, Skin loss, Third space
loss

Decreased cardiac output
chronic heart failure (CHF)

Renal vasoconstriction
Liver Disease, Sepsis, Hypercalcemia

Pharmacologic impairment of
autoregulation and GFR in specific settings
ACEi in bilateral renal artery stenosis, nonsteroidal
anti-inflammatory drugs (NSAIDs) in any renal
hypoperfusion setting

Large Renal Vessel Disease
Thrombo-embolic disease

Renal Microvasculature and Glomerular Disease
Inflammatory: glomerulonephritis, allograft rejection
Vasospastic: malignant hypertension, scleroderma crisis, preeclampsia, contrast
Hematologic: Hemolytic-Uremic Syndrome (HUS) &
Thrombocytopenic Purpura (TTP), Disseminated intravascular
coagulation

ATN
Ischemic
Toxic

Tubulo-interestitial Disease
Acute Interestitial Nephritis (AIN), Acute cellular allograft rejection,
viral (HIV, BK virus), infiltration (sarcoid)

Intratubular Obstruction
myoglobin, 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 valve
functional: anticholinergics, L-DOPA
Prostate disease;
Bladder disease;
anatomic: cancer, schistosomiasis
functional: 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)
2)
3)
4)
5)
Obtain a thorough history and physical;
review the chart in detail;
Do everything you can to accurately assess
volume status;
Always order a renal ultrasound;
Look at the urine;
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.





Antibiotics
Aminoglycosides (10-15% Incidence of
Acute Tubular Necrosis)
Occurs in 10-20% patients on 7 day
course
Results in non-oligurics; increased
Creatinine
A single dose early in septic course is
usually safe

Sulfonamides

Amphotericin B (Incidence 80-90%)

Levofloxacin

Ciprofloxacin

Rifampin

Tetracycline

Acyclovir (only nephrotoxic in
intravenous form)

AntiHyperlipidemics

Sulfonamides

Statins

Vasculitis reaction

Gemfibrozil

NSAIDs

Nephrotic Syndrome type reaction

Rifampin

Diuretics (Thiazides and furosemide)

Allopurinol
Serum Creatinine rise is reversible on
stopping Fenofibrate

Cimetidine

Ciprofloxacin

Chemotherapy

Dilantin

Cisplatin

Ifosphamide

Causes Fanconi's Syndrome

Miscellaneous Drugs

Chronic Stimulant Laxative use





Associated with Acute Renal Failure due
to Rhabdomyolysis
Fenofibrate (Tricor)
Increases Serum Creatinine without
significant decrease in GFR
Resulting chronic volume depletion and
Hypokalemia causes nephropathy

Pentamidine

Chemotherapy and Immunosuppressants

Cisplatin

Methotrexate

Mitomycin

Cyclosporine

NSAIDs

Heavy Metals

Aspirin

Mercury Poisoning


Lead Poisoning

Arsenic Poisoning

Bismuth

Lithium related kidney disorders


Polydipsia and Nephrogenic Diabetes
Insipidus
Radiographic contrast

ACE Inhibitors


Dialysis indications: Creatinine >2.5
or Seizures, ALOC, Rhabdomyolysis
Chronic kidney disease with fibrosis
Expect an increase of Serum Creatinine
in Chronic kidney disease
Low dose Aspirin reduces Renal function
in elderly
◦
Decreased Creatinine Clearance after
2 weeks of use
◦
Changes persisted for at least 3
weeks off Aspirin
Mesalamine (Asacol, Pentasa)
◦
Acute Renal Failure
◦


Mesalamine is an NSAID analog and
has systemic absorption from the
bowel

Penicillins and Cephalosporins

Hypersensitivity (fever, rash, arthralgia)

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, comorbidities (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):847-50
Am J Kidney Dis. 2007 Jan;40(1):56-68
Crit Care Med. 2006 Mar;34(3):707-14

Loop diuretics may convert an oliguric into a nonoliguric 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):2547-53
Crit Care Resusc. 2007 Mar;9(1):60-8

The most recent trials seem to confirm a
potential positive preventive effect of Nacetylcysteine (NAC), particularly in contrastinduced 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
challenge
SCr >1.5 mg/dl or GFR< 40 cc/min
Absence of proteinuria (<500 mg/d)
Other causes are rouled out (obstruction, ATN,
etc.)
Minor diagnostic criteria:
Urine volume < 400 cc/day
UNa < 10 meq/L
SNa < 130 meq/L
Urine 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




Disadvantages
Maximum solute
•Hemodynamic instability
clearance of 3
•Hypoxemia
modalities
•Rapid fluid and
electrolyte shifts
Best therapy for
severe hyperkalemia•Complex equipment
•Specialized personnel
Limited anti•Difficult in small infants
coagulation time
Bedside vascular
access can be used








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
Subcutaneous
coupling
External
segment
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.

Definitions
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

Definitions
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

Pathophysiology
•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 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.

Types
•Aortic dissection
•Pulmonary edema
•MI
•Acute coronary
syndrome
•Acute renal failure
•HELLP syndrome
•Severe preeclampsia
•Eclampsia
•Hypertensive
encephalopathy
•Subarachnoid hemorrhage
•Intracranial hemorrhage
•Acute ischemic stroke
•Sympathetic crisis

Target Organ Damage Associated with
Hypertensive 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 reestablished
•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 Reduction
•Acute renal deterioration
•Ischemic cardiac event
•Ischemic cerebral event
•Retinal artery occlusion (blindness)

Labetalol
•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.

Esmolol
•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.

Nicardipine
•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.

Nitroglycerin
•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.

Nitroprusside
•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

Phentolamine
•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

Fenoldopam
•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

Enalaprilat
•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:
•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
Symptoms:
Headache, Nausea/Vomiting, Lethargy,
Confusion, Lateralizing neurological symptoms
that are not often in an anatomical distribution.
Signs:
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
Therapy




Nitroprusside
◦ 1st line, 0.3 – 10 mcg/kg/minute
Labetalol
Enalaprilat
Fenoldopam
Pathophysiology


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 Symptoms


Abrupt and severe dyspnea, tachypnea, and
diaphoresis
Rales, wheezes, distant breath sounds, frothy
sputum, and gallop rhythm
Goals 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.
Therapy




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
Therapy




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