Mind map

Acute Kidney Injury

Gracelyn Hayden English

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Acute Kidney Injury

Clinical Manifestations
- 3 phases (Lewis et al., 2014)
  - Initiation (Lewis et al., 2014)
    - elevated serum creatinine (Lewis et. al, 2014)
    - Elevated BUN (Lewis et al., 2014)
    - Decrease in urine output (Lewis et al., 2014)
  - Maintenance (Lewis et al., 2014)
    - Anuric (Lewis et al., 2014)
    - Oliguric (Lewis et al., 2014)
      - Urinary changes (Lewis et al., 2014)
        Urine sediment which may contain RBCs, WBCs, casts and proteinuria (Lewis et al., 2014)
      - Fluid and electrolyte abnormalities (Lewis et al., 2014)
        Fluid overload (Lewis et al., 2014)
        Distended neck veins (Lewis et al., 2014)
        Edema (Lewis et al., 2014)
        Hypertension (Lewis et al., 2014)
        Untreated
        CHF (Lewis et al., 2014)
        Pulmonary edema (Lewis et al., 2014)
        Pleural and pericardial effusions (Lewis et al., 2014)
        Metabolic acidosis (Lewis et al., 2014)
        Kussmaul's respirations (Lewis et al., 2014)
        Lethargy (Lewis et al., 2014)
        If left untreated, pt can end up in a comatose state (Murphy et Byrne, 2010)
        Nausea and vomiting (Murphy & Byrne, 2010)
        Tachycardia (Murphy & Byrne, 2010)
        Intractable hiccups (Murphy & Byrne, 2010)
        Myocardial depression and vasodilation (Murphy & Byrne, 2010)
        Hypotension (Murphy & Byrne, 2010)
        Bradycardia (Murphy & Byrne, 2010)
        Hyponatremia (Lewis et al., 2014)
        Cerebral edema if untreated (Lewis et al., 2014)
        Hyperkalemia (Lewis et al., 2014)
        Tissue trauma (Lewis et al., 2014)
        Weakness (Lewis et al., 2014)
        Cardiac dysrhythmias (Lewis et al., 2014); Murphy & Byrne, 2010)
        GI absorption of calcium decreases (Lewis et al., 2014)
        Hypocalcemia (Lewis et al., 2014)
        Hyperphosphatemia (Lewis et al., 2014)
        Tetany (Lewis et al., 2014)
      - Blood changes (Lewis et al., 2014)
        Impaired erythropoietin production (Lewis et al., 2014)
        Anemia (Lewis et al., 2014)
        WBCs are altered (Lewis et al., 2014)
        Immunodeficiency (Lewis et al., 2014)
        Infections (Lewis et al., 2014)
        High mortality rate (Lewis et al., 2014)
      - Waste product accumulation (Lewis et al., 2014)
        Uremia (Lewis et al., 2014)
        Dysgeusia (Murphy & Byrne, 2010)
        Decreases platelet adhesiveness (Lewis et al., 2014)
        Internal bleeding (Lewis et al., 2014)
        Neurological changes (Lewis et al., 2014)
        Fatigue (Lewis et al., 2014)
        Seizures (Lewis et al., 2014)
        Stupor (Lewis et al., 2014)
        Coma (Lewis et al., 2014)
        Stomatitis (Lewis et al., 2014)
        Elevated BUN and creatinine (Lewis et al., 2014)
    - Nonoliguric (Lewis et al., 2014)
  - Recovery (Lewis et al., 2014)
    - BUN, creatinine and GFR return to normal (Murphy & Byrne, 2010)
    - Diuretic phase (Lewis et al., 2014)
      - Fluid and electrolyte abnormalities (Lewis et al., 2014)
        Hypovolemia (Lewis et al., 2014)
        Hypotension (Lewis et al., 2014)
      - Towards the end of the phase, acid/base, electrolyte and waste product lab values normalize (Lewis et al., 2014)
Assessments
- Volume Status (Murphy & Byrne, 2010)
  - Fluid overload (Murphy & Byrne, 2010)
    - Edema (Murphy & Byrne, 2010)
  - Dehydration (Murphy & Byrne, 2010)
    - Loss of skin elasticity and dry mouth (Murphy & Byrne, 2010)
    - Fluid losses (Lewis et al., 2014)
  - Urinary pattern (Murphy & Byrne, 2010)
- Infection
  - Pyrexia (Murphy & Byrne, 2010)
- Medications patient is currently taking
  - NSAIDS, ACE Inhibitors , Aminoglycosides, are potentially nephrotoxic (Murphy & Byrne,2010)
- Level of Consciousness (Gedeon, 2013)
- Vital signs
- ECG (Gedeon, 2013);(Murphy & Byrne, 2010)
  - Ventricular fibrillation (Murphy & Byrne, 2010)
  - Broadened QRS complex (Murphy & Byrne, 2010)
  - Tall tented T waves (Murphy & Byrne, 2010)
  - Prolonged P-R interval (Murphy & Byrne, 2010)
  - ST segment depression (Murphy & Byrne, 2010)
- Blood glucose (Murphy & Byrne, 2010)
- Inputs and Outputs (Gedeon, 2013)
- Urine (Lewis et al., 2014)
  - Colour (Lewis et al., 2014)
  - Specific gravity (Lewis et al., 2014)
  - Blood, protein and glucose (Lewis et al., 2014)
- If receiving RRT
  - Access site for inflammation (Lewis et al., 2014)
  - LOC (Lewis et al., 2014)
  - Dryness and inflammation in oral mucosa (Lewis et al., 2014)
  - Adventitious breath sounds (Lewis et al., 2014)
  - Extra heart sounds or murmurs (Lewis et al., 2014)
Etiology
- Primary (Gedeon, 2013)
  - 3 Injury Pathways (Gedeon, 2013)
    - Prerenal (Gedeon, 2013); (Lewis et al., 2014)
      - Reduced blood flow (Lewis et al., 2014)
        Decreased glomerular perfusion and filtration (Lewis et al., 2014)
        Low cardiac output (Lewis et al., 2014); (Murphy & Byrne, 2010)
        Decreased peripheral vascular resistance (Lewis et al., 2014)
        Vascular obstruction (Lewis et al., 2014)
        Hypovolemia (Lewis et al., 2014); (Murphy & Byrne, 2010)
        Hemorrhage (Murphy & Byrne, 2010)
        Bodily Fluid Losses (Murphy & Byrne, 2010)
        Blood Volume Redistribution (Murphy & Byrne, 2010)
        Vasoactive medications (Lewis et al., 2014)
        ACE inhibitors, ARBs, epinephrine and large doses of dopamine (Lewis et al., 2014)
    - Intrarenal (Intrinsic) (Gedeon, 2013); (Lewis et al., 2014)
      - Injury to renal tissue (Murphy & Byrne, 2010)
        Glomerular (Murphy & Byrne, 2010)
        Glomerulonephritis (Lewis et al., 2014); (Murphy & Byrne, 2010)
        Interstitial (Murphy & Byrne, 2010)
        Tubular (Murphy & Byrne, 2010)
        Ischaemia (Lewis et al., 2014); (Murphy & Byrne, 2010)
        Acute tubular necrosis (Lewis et al., 2014)
        Nephrotoxins (Murphy & Byrne, 2010)
        Intrinsic toxins (Murphy & Byrne, 2010)
        Hemoglobin (Lewis et al., 2014) (Murphy & Byrne, 2010)
        Myoglobin (Lewis et al., 2014) (Murphy & Byrne, 2010)
        Extrinsic toxins (Murphy & Byrne, 2010)
        Medications (Murphy & Byrne, 2010)
        Radiocontrast dye (Murphy & Byrne, 2010)
      - Injury To Vasculature (Murphy & Byrne, 2010)
    - Postrenal (Gedeon, 2013); (Lewis et al., 2014)
      - Obstruction of urinary flow (Lewis et al., 2014); (Murphy & Byrne, 2010)
        Kidney stones (Murphy & Byrne, 2010)
        Tumor (Murphy & Byrne, 2010)
        Trauma (Lewis et al., 2014)
        Benign prostatic hyperplasia (Lewis et al., 2014)
- Secondary (Gedeon, 2013)
Diagnostics and Labs
- Arterial Blood Gases (Murphy & Byrne, 2010)
- ESR and CRP (Murphy & Byrne, 2010)
- Blood and urine cultures (Murphy & Byrne, 2010)
- Urinalysis (Lewis et al., 2014)
- Renal ultrasound (Lewis et al., 2014)
- CT scan (Lewis et al., 2014)
- History and physical examination (Lewis et al., 2014)
- Serum creatinine and BUN (Lewis et al., 2014)
- Serum electrolytes (Lewis et al., 2014)
- Renal scan (Lewis et al., 2014)
- Retrograde pyelogram (Lewis et al., 2014)
Nursing Interventions
- Mouth care as mouth lesions can lead to respiratory infections (Murphy & Byrne, 2010)
- Cateter Care (Gedeon, 2013)
- Patient Teaching (Gedeon, 2013)
  - Strict Renal Diet (Gedeon, 2013)
  - S/S of AKI (Lewis et al., 2014)
- Venous Thromboembolism Prophylaxis (Bourbonnais et al., 2016); (Gedeon, 2013)
- Cardiac Monitoring (Gedeon, 2013)
- Psychosocial care (Lewis et al., 2014)
- Measuring intakes and outputs (Lewis et al., 2014)
  - Daily Weights (Gedeon, 2013)
- Aseptic technique to prevent infections (Lewis et al., 2014)
- Skin care to prevent pressure ulcers (Lewis et al., 2014)
Treatment and Collaborative Care
- Nutrition therapy (Murphy & Byrne, 2010)
  - enteral feeding best for critically ill (Murphy & Byrne, 2010)
  - Protein intake for negative nitrogen balance (Murphy & Byrne, 2010)
  - Potassium restriction (Murphy & BYrne, 2010)
  - Phosphate restriction (Murphy & Byrne, 2010)
  - Sodium restriction (Murphy & Byrne, 2010)
  - Calcium supplements or phosphate-binding agents (Lewis et al., 2014)
  - Adequate calories (Lewis et al., 2014)
- For hyperkalemia
  - Stabilize myocardium (Lewis et al., 2010)
    - Calcium gluconate IV (Lewis et al., 2014)
  - Shift potassium into cells (Lewis et al., 2014)
    - IV infusion or bolus of insulin or dextrose (Murphy & Byrne, 2010)
    - Salbutamol (Lewis et al., 2014)
    - Sodium bicarbonate (Lewis et al., 2014)
  - Enhance potassium removal (Lewis et al., 2014)
    - RRT if hyperkalemia is over 6.5 mmol/L (Murphy & Byrne, 2010)
    - Cation exchange resins such as Kayexalate and Calcium resonium (Lewis et al., 2014)
    - Loop diuretics such as furosemide (Lewis et al., 2014)
  - Long-term treatment (Lewis et al., 2014)
    - no potassium-sparing diuretics, ACE Inhibitors and ARBs (Lewis et al., 2014); (Murphy & Byrne, 2010)
    - potassium restricted in diet (Lewis et al., 2014); (Murphy & Byrne, 2010)
- To increase renal perfusion and address dehydration (Murphy & Byrne, 2010)
  - Volume Resuscitation (Murphy & Byrne, 2010)
    - Diuretic therapy (Lewis et al., 2014)
      - Loop diuretics (Lewis et al., 2014)
      - Osmotic diuretics (Lewis et al., 2014)
    - Volume expanders (Lewis et al., 2014)
- Renal Replacement Therapy (RRT). Indicated with renal insufficiency (Murphy & Byrne, 2010); (Wierstra, 2016)
  - Peritoneal dialysis (Murphy & Byrne, 2010)
  - Hemodialysis (Gedeon, 2013); (Murphy & Byrne, 2010)
    - Method of choice for rapid changes (Lewis et al., 2014)
  - Continuous renal replacement therapy (Bourbonnais et al., 2016) (Murphy & Byrne, 2010)
  - Sustained low-efficiency dialysis (SLED) (Murphy & Byrne, 2010)
- For radio contrast induced AKI
  - N-acetylcysteine (Lambert et al., 2017)
  - Ascorbic acid (Lambert et al., 2017)
  - Post-procedure hydration (Lambert et al., 2017)
- Transplantation (final resort) (Lewis et al., 2014)
Pathophysiology
- Decreases circulating blood volume (Lewis et al., 2014)
  - Increased angiotensin II, aldosterone, norepinperhine, and antidiuretic hormone (Lewis et al., 2014)
    - Blood flow preserved to essential organs (Lewis et al., 2014)
    - Less sodium excreted, increased salt and water retention and decreased urine output (Lewis et al., 2014)
      - Prerenal azotemia (Lewis et al., 2014)
- Hypovolemia and decreased renal blood flow (Lewis et al., 2014)
  - Renin release (Lewis et al., 2014)
    - Activates the renin-angiotensin-aldosterone system (Lewis et al., 2014)
      - Peripheral artieries and renal afferent arterioles constrict (Lewis et al., 2014)
  - Decreases glomerular capillary pressure and GFR (Lewis et al., 2014)
    - Oliguria (Lewis e t al., 2014)
- Ischemia (Lewis et al., 2014)
  - Decreases glomerular capillary permeability (Lewis et al., 2014)
    - Decreases GFR (Lewis et al., 2014)
      - Decreases blood flow (Lewis et al., 2014)
        Tubular dysfunction (Lewis et al., 2014)
- Damaged tubules (Lewis et al., 2014)
  - Interstitial edema (Lewis et al., 2014)
  - Necrotic epithelial cells accumulate (Lewis et al., 2014)
    - Decreases GFR (Lewis et al., 2014)
    - Increases intratubular pressure (Lewis et al., 2014)
- Glomerular filtrate leaks back into plasma (Lewis et al., 2014)
  - Decreases intrabular fluid flow (Lewis et al., 2014)
- Mechanical obstruction (Lewis et al., 2014)
  - Urine backflows into the renal pelvis (Lewis et al., 2014)
    - Kidney function impaired (Lewis et al., 2014)
- Kidneys cannot synthesize ammonia (Lewis et al., 2014)
  - serum bicarbonate used to buffer H+ (Lewis et al., 2014)
    - Serum bicarbonate level decreases (Lewis et al., 2014)
      - Metabolic acidosis occurs (Lewis et al., 2014)
Definition: Acute kidney injury is a sudden decline in kidney function, causing disturbances in fluid balance, electrolyte shifts, acid base imbalance, that causes a decline in the glomerular filtration rate, urine output and/or elevation in serum creatinine (Gedeon, 2013); (Lewis et al., 2014)
Risk factors
- Advanced age (Coelho et al., 2016); (Lewis et al., 2014)
- Trauma (Lewis et al., 2014)
- Surgical procedures (Lewis et al., 2014)
- Extensive burns (Lewis et al., 2014)
- Cardiac failure (Lewis et al., 2014)
- Sepsis (Lewis et al., 2014)
- Obstetrical complications (Lewis et al., 2014)
- Hypertension (Lewis et al., 2014)
- Diabetes mellitus (Lewis et al., 2014)