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Approach to the Critical Patient
Immediate priorities
Life threats to address first
Hemodynamic compromise driving hypoperfusion
MAP < 65 mmHg despite initial resuscitation
Shock physiology with mottling and oliguria
Refractory hyperkalemia
K+ > 6.0 mmol/l with ECG changes
Peaked T waves, QRS widening, or bradycardia
Severe metabolic acidosis
pH < 7.1
Rising anion gap with uremia
Pulmonary edema unresponsive to diuretics
Hypoxemia from volume overload
Consider urgent RRT
Restore renal perfusion early
Pre-renal AKI is rapidly reversible if corrected promptly
Prolonged hypoperfusion progresses to ischemic ATN
Window is hours to days
Identify and reverse the perfusion insult
Volume loss, sepsis, cardiac, or hepatorenal
Hold offending nephrotoxins
Monitoring and targets
Perfusion and renal targets
Mean arterial pressure
Target MAP >= 65 mmHg
Individualize higher in chronic hypertension
Urine output
Target > 0.5 ml/kg/hr
Foley for accurate hourly measurement
Volume status
Reassess after each fluid bolus
Avoid iatrogenic fluid overload
Monitoring bundle
Cardiac monitor for hyperkalemia
Continuous telemetry if K+ > 6.0 mmol/l
ECG with any potassium symptoms
Serial laboratory trend
Creatinine and potassium q6-12h
Bicarbonate and phosphate trend
Immediate consults and escalation
Escalation triggers
Failure to respond to volume challenge in 24-48h
Suggests intrinsic AKI or ATN
Reassess diagnosis
Indications for renal replacement therapy
Refractory hyperkalemia
Severe acidosis or uremic complications
Nephrology consultation
KDIGO Stage 3 AKI or need for RRT
Escalate early for dialysis planning
Vascular access coordination
AKI without clear etiology
Suspected glomerulonephritis or vasculitis
Pre-existing CKD stage 4 or worse
History
Presentation pattern
Volume loss history
Gastrointestinal losses
Vomiting
Diarrhea
Reduced intake
Poor oral intake or NPO status
Limited access to fluids
Other fluid losses
Hemorrhage, GI or surgical
Excessive sweating or burns
Urine output change
Oliguria
< 0.5 ml/kg/hr for >= 6 hours
KDIGO urine output criterion
Anuria
Suggests obstruction or severe ATN
Less typical of simple pre-renal
Causative context
Cardiac contributors
Heart failure features
Dyspnea and orthopnea
Peripheral edema
Decreased effective circulating volume
Cardiorenal physiology
Recent decompensation
Hepatic contributors
Cirrhosis features
Ascites and jaundice
Alcohol use
Hepatorenal physiology
Splanchnic vasodilation
Progressive azotemia
Infection and sepsis
Sepsis screen
Fever and chills
Identifiable source of infection
Septic vasoplegia
Most common ICU cause of AKI
Distributive shock physiology
Medications and baseline
Nephrotoxic and perfusion-altering drugs
Recent diuretic changes
Volume depletion risk
Dose escalation
ACE inhibitors or ARBs
Reduce efferent arteriolar tone
Hold during severe AKI
NSAIDs
Inhibit afferent arteriolar dilation
Common precipitant
Calcineurin inhibitors
Cyclosporine or tacrolimus
Renal vasoconstriction
Baseline kidney function and risk
Prior creatinine values
Essential for staging
Known CKD reduces reserve
Triple whammy combination
ACEi plus diuretic plus NSAID
High pre-renal AKI risk
Family history
Polycystic kidney disease
Hereditary nephropathy for baseline CKD
Physical Exam
Vital signs and volume status
Hemodynamic snapshot
Blood pressure
Hypotension
Orthostatic changes
Heart rate
Tachycardia as hypovolemia marker
MAP < 65 mmHg concerning
Perfusion signs
Delayed capillary refill
Mottling in shock
Hypovolemia findings
Mucous membranes
Dry oral mucosa
Reduced skin turgor
Jugular venous pressure
Flat JVP
Low filling state
Findings by cause
Decreased effective circulating volume
Heart failure signs
Elevated JVP
S3 gallop and crackles
Cirrhosis signs
Ascites and abdominal distension
Peripheral edema
Clues to alternative diagnoses
Skin findings
Rash suggesting interstitial nephritis or vasculitis
Livedo reticularis suggesting cholesterol emboli
Abdominal findings
Palpable bladder suggesting obstruction
Tenderness suggesting peritonitis
Bedside maneuvers
Fluid responsiveness assessment
Passive leg raise
Reversible preload challenge
Predicts response to fluids
Point-of-care ultrasound
IVC diameter and collapsibility
Lung B-lines for pulmonary edema
PITFALLS
Volume status can be deceptive
Hypervolemic states with low effective volume
Heart failure and cirrhosis appear fluid overloaded
Elderly atypical presentation
Confusion as primary symptom
Subtle volume depletion
Differential Diagnosis
Distinguishing pre-renal from intrinsic
Acute tubular necrosis
Urinary indices
FENa > 1%
Urine sodium > 40 mmol/l
Sediment and response
Muddy brown granular casts
Does not respond to volume challenge
Coding
ICD-10 N17.0
Ischemic or nephrotoxic injury
Pre-renal azotemia
Urinary indices
FENa < 1%
Urine sodium < 20 mmol/l
Coding
ICD-10 N17.9 acute kidney failure
SNOMED CT prerenal azotemia concept
Other categories
Post-renal obstruction
Imaging
Hydronephrosis on ultrasound
Distended bladder
Risk context
BPH or pelvic malignancy
Nephrolithiasis
Coding
ICD-10 N13.x obstructive uropathy
Bladder scan to exclude retention
Hepatorenal syndrome
Features
Cirrhosis with ascites
FENa < 1% but no response to albumin
Mechanism
Splanchnic vasodilation
Diagnosis of exclusion
Intrinsic renal disease mimics
Acute interstitial nephritis
Drug exposure with fever and rash
Eosinophiluria and WBC casts
Glomerulonephritis
RBC casts and proteinuria
Systemic vasculitis features
Rhabdomyolysis
Elevated CK and myoglobinuria
Heme-positive urine without RBCs
Cardiorenal syndrome
Acute decompensated heart failure
Elevated BNP
Venous congestion
Management distinction
Diuresis rather than volume loading
Relieve congestion
Laboratory Tests
Core renal labs
Basic metabolic panel
Creatinine
Compare to baseline for staging
Serial q6-12h in acute setting
Urea and ratio
BUN:Cr > 20:1 supports pre-renal
Reflects enhanced urea reabsorption
Potassium and bicarbonate
Hyperkalemia screen
Metabolic acidosis screen
Urinary diagnostic indices
Fractional excretion of sodium
FENa < 1% supports pre-renal
Pooled sensitivity 95%, specificity 91%
Most reliable in oliguric patients off diuretics
Fractional excretion of urea
FEUrea < 35% alternative when on diuretics
Moderate diagnostic accuracy
Spot urine chemistry
Urine sodium < 20 mmol/l
Urine osmolality > 500 mOsm/kg
Urinalysis and sediment
Urinalysis with microscopy
Sediment pattern
Bland or hyaline casts in pre-renal
Muddy brown casts in ATN
Concentration markers
Specific gravity > 1.020
High urine osmolality
Red flags on dipstick
Blood and protein suggesting glomerular disease
Leukocytes suggesting interstitial nephritis
Adjunct and monitoring labs
Targeted studies by suspicion
Lactate
Sepsis and hypoperfusion marker
>= 2 mmol/l concerning
Creatine kinase
Rhabdomyolysis screen
Dark urine context
Liver function tests
Hepatorenal assessment
Blood cultures if septic
Serial monitoring panel
Electrolyte trend
Potassium and bicarbonate
Phosphorus and calcium
Hemoglobin
Anemia of blood loss
Baseline for transfusion need
Diagnostic Tests
Scoring Systems
KDIGO AKI staging
Stage 1
SCr rise >= 26.5 micromol/l within 48h or 1.5-1.9x baseline
Urine output < 0.5 ml/kg/hr for 6-12h
Stage 2
SCr 2.0-2.9x baseline
Urine output < 0.5 ml/kg/hr for >= 12h
Stage 3
SCr >= 3.0x baseline or >= 353.6 micromol/l or RRT initiation
Urine output < 0.3 ml/kg/hr for >= 24h or anuria >= 12h
Diagnostic indices and tools
FENa calculator
Key tool to separate pre-renal from intrinsic
Requires paired urine and serum sodium and creatinine
Novel biomarkers
NGAL and TIMP-2 x IGFBP-7
Detect tubular injury before creatinine rises, limited availability
MRI
MRI role in AKI
Limited acute utility
Not routine for pre-renal AKI
Time and availability constraints
Problem-solving indications
Renal vein thrombosis evaluation
Mass or vascular anomaly characterization
Contrast caution
Avoid gadolinium in severe AKI
Nephrogenic systemic fibrosis risk with low GFR
CT
CT abdomen and pelvis
Indications
Obstruction suspected but ultrasound equivocal
Not routinely needed in clear pre-renal
Findings
Hydronephrosis or obstructing stone
Retroperitoneal or pelvic mass
Contrast considerations
Weigh contrast-associated nephropathy risk
Non-contrast protocol for stone search
Evidence note
Imaging unnecessary when picture clearly pre-renal
Rapid response to volume supports diagnosis
Reserve CT for diagnostic uncertainty
Ultrasound
Renal ultrasound
Primary indication
Exclude obstruction with hydronephrosis
Recommended in most AKI patients
High-yield populations
Older males with BPH
Pelvic malignancy or single kidney
Expected pre-renal findings
Normal-appearing kidneys
No hydronephrosis
Point-of-care ultrasound
Volume assessment
IVC diameter and collapsibility
Fluid responsiveness estimate
Congestion assessment
Lung B-lines for pulmonary edema
Integrate with clinical exam
Disposition
Level of care selection
Admission indications
Stage 2 or 3 AKI
KDIGO staging threshold
Rising creatinine trajectory
Hemodynamic instability
Ongoing volume loss
Vasopressor requirement
Dangerous electrolyte or acid-base state
K+ > 6.0 mmol/l
Significant metabolic acidosis
Oliguria or anuria not responding to resuscitation
Failed initial fluid challenge
Underlying cause needing inpatient care
ICU and RRT indications
Refractory shock
Vasopressor-dependent
Rising lactate despite resuscitation
Renal replacement therapy needs
Refractory hyperkalemia or acidosis
Pulmonary edema or uremic complications
Discharge and follow up
Discharge criteria
Creatinine trending toward baseline
Improving after ED fluids
Stable electrolytes
Clinical stability
Adequate urine output
Tolerating oral intake
Reversible cause identified
Correctable precipitant
Reliable follow-up arranged
Follow-up plan
Repeat BMP
Within 48-72h for mild pre-renal AKI
Monitor for ongoing decline
Clinician follow-up
PCP or nephrology within 1-2 weeks
Medication reconciliation
Treatment
Initial stabilization
Hemodynamic resuscitation
Perfusion target
MAP >= 65 mmHg
Individualize in chronic hypertension
Access and monitoring
Establish IV access
Foley for urine output tracking
Vasopressor support if vasoplegia
Norepinephrine first-line
Start 0.05 mcg/kg/min IV infusion
Titrate every 5-10 min to MAP >= 65 mmHg
No fixed maximum, escalate per response
Reserve for fluid-refractory shock
After adequate volume given
Distributive or septic physiology
Volume resuscitation
Fluid selection and dosing
Balanced crystalloid preferred
Lactated Ringer or Plasma-Lyte over 0.9% saline
Reduces RRT and acidosis risk
Bolus strategy
250-500 ml boluses with reassessment
Goal euvolemia, not hypervolemia
Reassess volume status after each bolus
Avoid harmful fluids
No synthetic colloids such as hydroxyethyl starch
Increased RRT risk
Cause-specific volume strategy
Cirrhosis
Albumin 1 g/kg IV
Maximum 100 g/day
Cardiorenal syndrome
Diuresis rather than volume loading
Relieve venous congestion
Hemorrhage
Blood products for active bleeding
Source control
Medication management
Discontinue offending agents
Hold nephrotoxins
NSAIDs
ACE inhibitors and ARBs
Hold volume-depleting agents
Diuretics unless volume overloaded
Loop diuretics not used to treat pre-renal AKI
Renal dose adjustment
Adjust all renally cleared drugs
Review for accumulating nephrotoxins
Diuretic caution
Loop diuretics
Only for established volume overload
Do not improve renal recovery
Fenoldopam
Not supported for AKI prevention or treatment
Cochrane evidence does not show benefit
Hyperkalemia management
Membrane stabilization
Calcium gluconate 10%
10 ml IV over 2-3 minutes for ECG changes
Repeat if ECG changes persist
Onset 1-3 minutes, no effect on serum K+
Intracellular potassium shift
Insulin with dextrose
10 units regular insulin IV
With 25 g dextrose to prevent hypoglycemia
Monitor glucose for 4-6 hours
Salbutamol nebulized
10-20 mg nebulized
Additive intracellular shift
Sodium bicarbonate
Only if concurrent metabolic acidosis
Adjunctive shift effect
Potassium elimination
Binders
Sodium zirconium cyclosilicate or patiromer
Onset slower, definitive removal
Dialysis
For refractory hyperkalemia
Definitive removal when binders inadequate
Treat underlying cause
Cause-directed therapy
Sepsis
Source control
Early appropriate antibiotics
Cardiogenic shock
Inotropes or vasopressors
Optimize cardiac output
Ongoing monitoring
Urine output hourly
Target > 0.5 ml/kg/hr
Trend response to therapy
Laboratory cadence
Serial BMP q6-12h
Daily weights for fluid balance
Special Populations
Pregnancy
Pregnancy considerations
Physiologic baseline shift
GFR increased, baseline creatinine lower
Creatinine > 70 micromol/l may be abnormal
Pregnancy-specific causes
Hyperemesis gravidarum volume loss
Preeclampsia and HELLP overlap
Management adjustments
Avoid ACE inhibitors and ARBs
Balanced crystalloid resuscitation
Imaging approach
Ultrasound first-line
Avoid gadolinium and limit CT contrast
Geriatric
Older adult features
Increased susceptibility
Predisposition to hypovolemia
Renal artery atherosclerosis
Atypical presentation
Confusion as primary symptom
Blunted thirst response
Polypharmacy risk
Triple whammy combination common
Careful medication reconciliation
Reduced reserve
Lower baseline GFR
Higher progression to CKD
Pediatrics
Pediatric differences
Common precipitants
Gastroenteritis with dehydration
Diabetic ketoacidosis volume loss
Weight-based resuscitation
Crystalloid bolus 10-20 ml/kg
Reassess after each bolus
Staging adaptation
pRIFLE and KDIGO pediatric criteria
Estimate GFR with Schwartz equation
Medication safety
Avoid NSAIDs in dehydration
Weight-based renal dose adjustment
Background
Epidemiology
Frequency and burden
Most common cause of AKI
About 70% of community-acquired AKI
About 40% of hospital-acquired AKI
Sepsis as leading driver
47% of severe AKI cases in ICU
Highest mortality subgroup
Long-term consequences
Roughly 9x pooled risk of CKD
Roughly 2x risk of premature death
Pathophysiology
Mechanism of injury
Reduced renal perfusion
Structurally intact kidneys
Functional decline in GFR
Autoregulatory compensation
Afferent arteriolar dilation via prostaglandins
Efferent constriction via angiotensin II
Drug-mediated failure of autoregulation
NSAIDs block afferent dilation
ACEi and ARBs block efferent constriction
Progression pathway
Reversibility window
Rapidly reversible with restored perfusion
Preserved tubular function
Transition to ATN
Prolonged ischemia injures tubules
Longer recovery and higher morbidity
Therapeutic Considerations
Core principles
Perfusion restoration is the treatment
Correct the underlying insult
Avoid over-resuscitation
Avoid further injury
Remove nephrotoxins
Dose-adjust renally cleared drugs
Cause-tailored strategy
Hypovolemia
Balanced crystalloid
Titrate to euvolemia
Cirrhosis
Albumin expansion
Different from crystalloid approach
Cardiorenal
Decongestion over volume loading
Optimize forward flow
Patient Discharge Instructions
copy discharge instructions
Acute kidney injury home care
Drink fluids as advised to stay hydrated
Take only medications approved by your clinician
Do not restart held blood pressure or water pills until cleared
Avoid ibuprofen, naproxen, and other anti-inflammatories
Sick-day rules
Hold blood pressure pills and water pills during dehydrating illness
Resume only after clinician review
Seek care if unable to keep fluids down
Warning signs to return to ER
Little or no urine
Persistent vomiting or diarrhea with inability to keep fluids down
Confusion or excessive drowsiness
Chest pain or severe shortness of breath
Muscle weakness or palpitations
Swelling of legs, face, or abdomen
Follow up
Blood test to recheck kidney function within 2-3 days
Clinician or kidney specialist visit within 1-2 weeks
Bring an updated list of all medications
References
Guidelines and key sources
Guideline sources
KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury
AGA Clinical Practice Update on AKI in cirrhosis
AHA guidance on hyperkalemia and ECG monitoring
Landmark and evidence sources
Meta-analyses on fractional excretion of sodium and urea diagnostic performance
NEJM reviews on acute renal failure and kidney replacement therapy
Lancet reviews on acute kidney injury epidemiology and outcomes
Coding standards
ICD-10 N17.9 acute kidney failure unspecified
SNOMED CT prerenal azotemia disorder concept
SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.