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renal 2

VAN assessment for Large Vessel Occlusion (LVO)

  • The first true criterion to proceed with VAN: look for arm weakness. If there is arm weakness, you move forward with the VAN assessment; if there is no arm weakness, VAN assessment is less likely to indicate LVO (though not all-inclusive). The key trigger in VAN is the presence of arm drift.
  • VAN assessment sequence and meanings:
    • V (Vision): If there is vision disturbance (e.g., double vision or loss of a visual field), this supports LVO.
    • A (Aphasia): If the patient has a language problem (inability to understand commands, inability to articulate, or impaired language processing), this supports LVO.
    • N (Neglect): Includes signs like gaze deviation (gaze to one side) which can be associated with neglect. Note: gaze deviation is sometimes tested as part of the end assessment, not strictly during vision testing.
  • Practical execution notes:
    • If left-sided arm drift is observed, you check vision first; you then proceed to assess aphasia and neglect to refine LVO likelihood.
    • If vision is normal, you move on to aphasia; if aphasia is normal, you move to neglect; each abnormal finding pushes toward LVO.
  • Important caveat:
    • This VAN approach is not all-inclusive; it is a practical, one-pocket tool to quickly screen for potential LVO before imaging.

Prerenal AKI (Acute Kidney Injury) – overview and pathophysiology

  • Definition and basic mechanism:

    • AKI caused by reduced renal perfusion; low blood flow to the kidneys leads to impaired filtration.
    • Can result from absolute fluid loss (dehydration) or relative fluid loss (decreased effective circulating volume). It can also be caused by renal artery stenosis or embolus that reduces renal blood flow.

  • Classic scenario described:

    • A patient with tachycardia (e.g., ventricular tachycardia with a pulse) who is hypotensive can precipitate prerenal AKI due to decreased renal perfusion.

  • RAAS cascade (why blood pressure matters for kidneys):

    • Renin release from the juxtaglomerular cells in response to low renal perfusion initiates a cascade.
    • Angiotensin-converting enzyme (ACE) in the lungs converts Angiotensin I to Angiotensin II, a potent vasoconstrictor.
    • Angiotensin II constricts efferent arterioles (and other vasculature), increasing glomerular filtration pressure.
    • Aldosterone promotes sodium and water reabsorption, increasing intravascular volume and blood pressure.
    • Aldosterone also increases urea reabsorption, which raises BUN levels; overall, this helps maintain perfusion but can worsen renal injury if perfusion remains low.

  • Key hemodynamic target:

    • Maintain mean arterial pressure (MAP) to ensure renal perfusion: MAP > 65\,mmHg

  • Diagnostic clue (BUN/Creatinine):

    • In prerenal AKI, the body reabsorbs urea, leading to a higher BUN relative to creatinine.
    • If only BUN rises (creatinine remains near baseline), think prerenal; if both BUN and creatinine rise together (and increasingly), this points toward intrarenal injury (as filtration worsens).
    • Expression from transcript: a BUN/Creatinine ratio of about 40:1 would suggest prerenal; when both BUN and creatinine rise because filtration is impaired, it points toward intrarenal involvement.

  • Initial management considerations:

    • Treat hypotension and hypoperfusion with fluids (unless there are contraindications such as pulmonary edema or other fluid overload conditions).
    • In a rhythm abnormality with hypotension (e.g., hypotensive VTach), perform synchronized cardioversion. Typical energy settings discussed: E = 100\,\text{J}, with up to E = 120\,\text{J} if needed.
    • If MAP cannot be maintained, consider escalating therapies and addressing the underlying cause (hemorrhage, sepsis, etc.).

  • Clinical significance:

    • Prerenal AKI can progress to multiorgan dysfunction syndrome (MODS) if perfusion remains inadequate; the kidneys are a major organ affected by shock and hypoperfusion.
    • The kidneys’ response to hypoperfusion is crucial because a sustained low MAP can compromise renal function and contribute to downstream organ failure.

Intrarenal AKI – causes and mechanisms

  • When the problem originates inside the kidney (intrarenal), several etiologies are discussed:
    • Prerenal AKI can progress to intrarenal injury if hypoperfusion persists and renal cells die, worsening kidney function.
    • Nephrotoxins that injure nephrons (e.g., certain antibiotics, heavy metals like lead) can cause intrarenal damage.
    • Antifreeze ingestion historically caused intrarenal kidney failure when metabolized by the liver; modern management focuses on avoiding such toxins and leveraging other supportive treatments.
    • Uric acid buildup (e.g., in cancer therapy or high uric acid states) can damage nephrons.
    • Myoglobinuric nephropathy from rhabdomyolysis (muscle breakdown) is a major intrarenal cause discussed here.
    • Glomerulonephritis (inflammation of the glomerulus) can cause hematuria and proteinuria due to increased permeability of the glomerular capillary wall.
    • Pyelonephritis (infection of the kidney itself) is another intrarenal etiology.
    • Acute tubular necrosis (ATN): death of tubular epithelial cells leading to obstruction (sloughing cells) within tubules and impaired filtrate formation.
  • Mechanisms and clinical clues:
    • Rhabdomyolysis: widespread muscle injury releases myoglobin; myoglobin can damage renal tubules, leading to dark cola-colored urine and intrarenal injury.
    • Nephrotoxins: certain antibiotics, NSAIDs, heavy metals, and other toxins can injure nephrons directly.
    • Glomerular inflammation (glomerulonephritis): hematuria (blood in urine) is a key clue; proteinuria (often foamy urine) signals increased protein loss in urine.
    • Uric acid nephropathy: uric acid buildup can obstruct tubules and damage nephrons.
  • Important manifestations and signs:
    • Oliguria or anuria (reduced urine output) occurs with prerenal, intrarenal, and postrenal AKI.
    • Hematuria indicates glomerular injury; dark urine with myoglobin indicates rhabdomyolysis; foamy urine suggests proteinuria.
    • Protein in urine (proteinuria) is often foamy; albumin is the most common protein detected in urine in many cases.
  • Practical management notes (intrarenal focus):
    • If rhabdomyolysis suspected, aggressive IV fluids are key to diluting myoglobin and protecting kidneys; monitor for fluid overload.
    • If there is evidence of rhabdomyolysis with pulmonary edema or fluid overload risk, fluids may need to be balanced carefully.
    • For suspected ATN or glomerulonephritis, address the underlying cause, monitor electrolytes (especially potassium), and consider renal replacement therapy if indicated.
    • NSAID use and other nephrotoxins should be reviewed and avoided when possible to limit further damage.
  • Diagnostic considerations:
    • Hematuria and proteinuria point toward intrinsic kidney pathology (glomerular or tubular); presence of myoglobin in urine points toward rhabdomyolysis.
    • Indices such as BUN and creatinine typically rise with both prerenal and intrinsic renal injuries, but their relative changes help differentiate etiologies (see prerenal vs intrarenal discussion).

Postrenal AKI – obstruction to outflow

  • Core idea:
    • Postrenal AKI results from obstruction to urine outflow anywhere along the urinary tract, from the level of the bladder up to the kidneys.
  • Common causes described:
    • Prostate issues (e.g., benign prostatic hyperplasia, prostate cancer) can compress the urethra and impede urine outflow.
    • Bladder outlet obstruction such as large bladder after overfilling (as in the case with 2 L drained by Foley) or neurogenic bladder (nerve issues causing inability to void).
    • Ureteral obstruction from tumors or stones.
    • Other obstructive etiologies include neurogenic bladder dysfunction and post-surgical changes.
  • Case highlights (postrenal AKI):
    • A 65-year-old man presented in a primary care setting with urinary retention later found to be related to BPH; a Foley drained about 2 liters, indicating significant retention and postrenal obstruction.
  • Management principles:
    • The primary treatment is relief of obstruction (e.g., catheter drainage, addressing urinary retention, urology involvement).
    • In the prehospital setting, aggressive fluids may be avoided if there is a clear obstruction and risk of edema; instead, focus on airway, breathing, and supportive care while arranging definitive treatment.
    • Consider the overall clinical picture, including edema and respiratory status.
  • Prognosis and interventions:
    • Once obstruction is relieved, renal function may recover if injury is not advanced; however, persistent obstruction can lead to ongoing damage.
    • In persistent or severe cases, dialysis may be considered if renal function does not recover or if there are other indications for renal replacement therapy.

Case discussions and applied scenarios

  • Case 1: Four-year-old female with four days of worsening cough and dyspnea, plus one day of anuria and dark-colored urine; prior urgent care visit for cough and sore throat treated with amoxicillin.
    • Vitals and findings described:
    • Respirations around 70/min (tachypnea for a child).
    • Periorbital edema; coarse crackles bilaterally on lung auscultation; edema present.
    • Metabolic acidosis noted (acidemia).
    • Dark-colored urine suggesting possible rhabdomyolysis or glomerular/intrarenal pathology.
    • Diagnostic reasoning and differential:
    • Initial thought toward prerenal AKI due to decreased perfusion; however, the presence of edema, crackles, and dark urine shifted consideration toward intrarenal causes.
    • In discussion, intrarenal etiologies such as glomerulonephritis (e.g., post-infectious glomerulonephritis after strep), rhabdomyolysis, nephrotoxins, and ATN were considered.
    • Therapeutic debate and plan:
    • Fluid management was debated: fluids could help rhabdomyolysis but could worsen pulmonary edema or kidney injury in this context.
    • Lasix (furosemide) discussion: not expected to resolve the underlying injury if kidneys are not filtering well.
    • Respiratory support prioritized due to dyspnea and crackles; discussed options included noninvasive ventilation approaches (CPAP) or using baby VMS with PEEP if a mask for a four-year-old is not readily available.
    • If hypoxia worsens or kidney function deteriorates, dialysis could be considered as a potential intervention.
    • Key monitoring and actions:
    • Assess potassium level (hyperkalemia risk with AKI); consider obtaining a 12-lead ECG to evaluate hyperkalemia risk.
    • Continuous reassessment and timely communication with pediatric nephrology or the receiving hospital.
  • Case 2: Sixty-five-year-old male at a primary care visit with dizziness and headache; stroke assessment performed; high blood pressure; later hospitalized with a Foley catheter showing 2 L of urine drained.
    • Clinical interpretation:
    • The large-volume urine drainage at catheterization indicates significant urinary retention, consistent with postrenal AKI due to obstruction (e.g., BPH).
    • Management approach:
    • In the field, focus on airway/breathing/circulation and avoid excessive fluids if there is edema or respiratory compromise.
    • Plan for definitive management to relieve obstruction (urology involvement) and monitor renal function.
    • Evaluate for hyperkalemia and electrolyte disturbances requiring treatment; perform a 12-lead ECG if indicated.
    • In-hospital management may involve dialysis if kidney function fails to recover or to manage fluid overload and electrolyte abnormalities.

Key metabolic and electrolyte considerations in AKI

  • Hyperkalemia risk in AKI:
    • Reduced filtration leads to potassium retention; surveillance with ECG and labs is essential.
    • Management involves treating the underlying AKI, monitoring, and targeted therapies as indicated by ECG changes and potassium level.
  • Renal replacement therapy considerations:
    • Dialysis may be used in severe AKI (e.g., to control hyperkalemia, volume overload, uremic symptoms, or when kidneys fail to recover).
    • In pediatric and adult cases alike, dialysis can be used as an acute, short-term intervention to stabilize patients while addressing the underlying cause.

Physiologic mechanisms and clinical implications to remember

  • MAP and renal perfusion:
    • Maintaining MAP > 65 mmHg is crucial to preserve renal blood flow and avoid AKI progression.
  • Fluid management principles in AKI:
    • Fluid rescue is beneficial in rhabdomyolysis to prevent myoglobin-induced renal injury but must be balanced against risks of fluid overload and pulmonary edema.
  • RAS (Renin-Angiotensin System) physiology:
    • The RAAS cascade is activated by low renal perfusion, leading to vasoconstriction and aldosterone-mediated volume expansion to restore BP.
    • Pharmacologic inhibitors of RAAS (ACE inhibitors, ARBs) affect this system; ACE inhibitors have the suffix "-pril" (e.g., lisinopril).
  • Urinalysis clues and kidney injury localization:
    • Hematuria points toward glomerular disease or urinary tract injury; proteinuria and foamy urine suggest protein leakage; dark urine may indicate myoglobin or hematuria depending on context.
    • A urinalysis can help differentiate intrarenal (glomerular/nephron) from prerenal or postrenal etiologies when interpreted with clinical data.

Quick takeaways for exam preparation

  • VAN assessment:
    • Arm weakness is the first trigger; follow with vision, aphasia, and neglect testing to assess for LVO.
  • AKI etiologies categorized by location:
    • Prerenal: perfusion problem; treat with hemodynamic optimization; MAP > 65; potential progression to intrarenal injury if prolonged.
    • Intrarenal: nephrotoxins, rhabdomyolysis, glomerulonephritis, ATN, pyelonephritis; manage underlying cause and support kidneys; consider fluids for rhabdo but watch for overload.
    • Postrenal: obstruction to outflow (BPH, stones, neurogenic bladder); relieve obstruction.
  • Case-based reasoning:
    • Pediatric case emphasized careful balance between fluids and renal protection, respiratory support, and potential dialysis planning.
    • Adult postrenal case emphasized recognizing urinary retention with high-volume drainage and prioritizing obstruction relief with supportive care.
  • Diagnostics and monitoring:
    • Monitor MAP, urine output (oliguria/anuria), BUN/creatinine, potassium, and urinalysis findings (hematuria, proteinuria, myoglobin).
    • Use imaging and labs to differentiate prerenal vs intrarenal vs postrenal etiologies and guide management.