HYHO AKI Flashcards

1
Q

What is the definition/parameters of Acute Kidney Injury?

A

Acute Kidney Injury: Increase in serum creatinine of ≥ 0.3 mg/dL within 48 hours or within 7 days OR urine output of < 0.5mL/kg/hour for > 6 hours.

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2
Q

What is cardiorenal syndrome?

A

Cardiorenal syndrome is a condition in which therapy to relieve congestive symptoms of HF is limited by a decline in renal function as manifested by reduction in GFR. There is a bidirectional interaction between the heart and kidneys

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3
Q

Why is using creatine levels to calculate GFR slightly misleading in elderly populations?

A

-GFR is calculated using creatinine, which may underestimate the degree of dysfunction. For example, a frail elderly person has lower muscle mass therefore may have renal insufficiency with normal or only mild elevation of creatinine

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4
Q

What are the symptoms & signs associated with Acute Kidney Injury (AKI)?

A

decreased urine output

  • worsening dyspnea including dyspnea at rest, orthopnea and/or paroxysmal nocturnal dyspnea (PND)
  • worsening edema moving from dependent edema to anasarca and/or ascites
  • tachycardia, S3,
  • hypotension
  • JVD
  • liver distention and/or tenderness with palpation
  • Distended abdomen: fluid wave, and/or puddle sign to assess for ascites
  • skin tenting is best evaluated by pinching the skin of the forehead. The skin of a dehydrated patient will remain elevated rather than springing back to it’s original position.
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5
Q

What does a fluid wave detect?

A

-Fluid wave detects large volumes of free intrabdominal fluid. It has a specificity of 80-90%; a positive finding rules in ascites. However, its sensitivity is ~50%, so a negative test does not exclude ascites (i.e. it is volume dependent).

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6
Q

How does one perform a fluid wave?

A

The patient places the ulnar surface of their hand along the abdominal vertical midline. The operator places one hand on one flank and taps gently on the opposite flank. A positive sign when the operator feels a moderate to strong fluid wave emanating into the contralateral side.

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7
Q

What is a puddle sign?

A

-Puddle sign: It has a sensitivity of ~40 – 50% especially with small amounts of ascites. Positioning the patient makes it very difficult to evaluate.

This is an auscultatory percussion sign that requires the patient to support themselves on their hands and knees for 5 minutes. The operator then listens with the diaphragm while flicking a finger over a localized flank area of the abdomen starting at the lowest point and moving over to the opposite flank. A positive sign is when there is a sudden increase in intensity and clarity of the sound, signaling that the stethoscope has passed the edge of the peritoneal fluid.

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8
Q

What is anasarca?

A

-Anasarca is severe generalized edema that extends from the lower extremity proximally. It can cause ascites as well as subcutaneous edema; associated with heart failure, cirrhosis, severe malnutrition and renal failure.

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9
Q

What is paroxysmal nocturnal dyspnea?

A

-PND describes episodes of sudden dyspnea and orthopnea that awaken patient from sleep, prompting the patient to sit up or stand up. There may be associated wheezing and coughing. PND may be mimicked by nocturnal asthma attacks.

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10
Q

What is the sympathetic and parasympathetic innervation to the kidney and upper ureters?

A
Kidney
Sympathetics: T10-11
Parasympathetic – vagus nerve
Ureters – upper
Sympathetics: T10-11
Parasympathetics: vagus nerve
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11
Q

What is the sympathetic and parasympathetic innervation to the bladder and lower ureters?

A

Ureters – lower
o Sympathetics: T12-L2
o Parasympathetics: pelvic splanchnic nerve

Bladder
o Sympathetics: T12-L2
o Parasympathetics: pelvic splanchnic nerve

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12
Q

What are the chapmans points of the kidney?

A

Chapman Points
o Kidney
Anterior: one inch lateral and one inch superior to the umbilicus
Posterior: between the transverse process of T12 and L1 (on the ipsilateral side)

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13
Q

As part of the 5 Model Approach, what would the biomechanical approach be to a patient with AKI?

A
5 Model Approach
Biomechanical:
SD of OA, AA
SD of thoracic spine at viscerosomatic levels (T10-11)
SD of the psoas muscles
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14
Q

As part of the 5 Model Approach, what would the respiratory/circulatory approach be to a patient with AKI?

A

5 Model Approach
Respiratory/Circulatory
O2 via mask/nasal canula
-Lymphatics
o Thoracic inlet MFR
o Diaphragms (thoracolumbar, pelvic)
o Thoracic area: pectoral traction, doming the diaphragm, thoracic pump
o Abdominal area: abdominal pump, sacral rocking, pelvic diaphragm
o Extremities: effleurage, petrissage, pedal pump
o Rib raising

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15
Q

As part of the 5 Model Approach, what would the Metabolic/Energetic/Immune approach be to a patient with AKI?

A
Metabolic/Energetic/Immune
 Loop diuretics
 Fluid restriction
 Remove offending agents like NSAIDs, PPI
 Adjust meds based on renal function
 Monitor I/O’s, weights
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16
Q

As part of the 5 Model Approach, what would the behavioral approach be to a patient with AKI?

A
Behavioral
 Exercise
 Diet – restrict fluids
 Avoid offending agents
 Better management of CHF (inciting cause)
17
Q

What is the treatment for AKI?

A

TREATMENT:

  1. Remove offending agents: NSAIDS, PPI, etc.
  2. Judicious use of loop diuretics (furosemide)
  3. Adjust medication dosing based on renal function
  4. Supportive care: oxygen
  5. Monitor weight, I’s & O’s
  6. Fluid restriction
  7. Monitor electrolytes (Na+, K+, Ca+, Mg+, etc.)
  8. Case management/manager
  9. Dietary consult
18
Q

What is the long-term management of AKI?

A

Long-term MANAGEMENT:
1. Discussion with patient regarding personal wishes regarding Dialysis (both short and long-term), as well as other end-of-life matters such as Living Will and DPAHC.

  1. Avoid nephrotoxic drugs, including OTC preparations such as NSAIDs, PPI, etc.
  2. Regular monitoring of electrolytes, patient weight, fluid status, etc.
19
Q

What are the possible complications of AKI?

A

Complications:
Progression to oligouria or anuria: Dialysis (Renal Replacement Therapy) may be ‘initiated emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist,’ per the KDIGO guidelines. RRT should be continued until renal function is recovered or because continued provision of renal support is no longer consistent with the overall goals of care for the patient

20
Q

Why is a Living Will (LW) or Durable Power of Attorney for Healthcare (DPAHC) important in the care of a patient?

A
  • Living Will: summarizes choices about future medical care; typically addresses resuscitation and life support, but may include other preferences about treatments (feeding tube, dialysis, intubation/ventilator support).
  • Durable Power of Attorney for Healthcare (DPAHC) authorizes another person (or surrogate) to make decisions on the patient’s behalf.
21
Q

What is advance care planning and why is it important?

A

Advance care planning:

This permits patients to talk to their physicians and families regarding end-of-life issues. It often takes more than one visit, so a team approach (interprofessional) involving case managers and/or nursing staff. The role of the physician is to provide information about prognosis and treatment options to help a patient formulate preferences based on risk-benefit analysis and the patient values. The patient choices may change with time and change in health status, so the documents can be reviewed and updated as necessary.

22
Q

-If a patient has elected some restriction (do not resuscitate, do not intubate, etc.) in their Living Will, the physician MUST do what appropriately?

A

-If a patient has elected some restriction (do not resuscitate, do not intubate, etc.) in their Living Will, the physician MUST document the order appropriately. The presence of the LW alone will not prevent resuscitation.

23
Q

What is neurohumoral adaptation?

A

Neurohumoral adaptations: in the setting of HF, hemodynamic derangements trigger activation of the sympathetic nervous system and RAAS and increases in the release of vasopressin (andidiuretic hormone) and endothelin-1, which promote salt and water retention and systemic vasoconstriction. These pathways lead to disproportionate reabsorption of urea compared with that of creatinine. They also overwhelm the vasodilatory and natriuretic effects of natriuretic peptides, nitric oxide, prostaglandins, and bradykinin. The systemic vasoconstriction increases cardiac afterload which reduces cardiac output, can further reduce renal perfusion.

24
Q

What is increased renal venous pressure?

A

Increased renal venous pressure: Increases in intra-abdominal or central venous pressure, which should increase renal venous pressure, reduces GFR. In other words, there is an inverse relationship between central venous pressure and GFR. However, the mechanism by which renal venous pressure might lead to reduction in GFR is not well understood

25
Q

How is HFpEF related to AKI?

A

Associations with heart failure with preserved ejection fraction (HFpEF): renal dysfunction can lead to metabolic derangements resulting in systemic inflammation and microvascular dysfunction, which can cause cardiomyocyte stiffening, hypertrophy and interstitial fibrosis. Exact relationships are not well understood.

26
Q

-Normal urine output can be maintained even in the face of low ____. The ability for diuretic use to improve output is a good prognosis. ______ diuretics are the mainstay of treatment

A

-Normal urine output can be maintained even in the face of low GFR. The ability for diuretic use to improve output is a good prognosis. Loop diuretics (i.e. furosdemide) are the mainstay of treatment