Emergencies in Renal Failure and Dialysis Patients

Tintinalli chapter 93

• ESRD: irreversible loss of renal function, accumulation of toxins and loss of internal homeostasis.

• Uremia: clinical syndrome resulting from ESRD.

Epidemiology

• 1999=89,252 new cases/424,179 patients being tx for ESRD

• Causes: DM=#1, HTN=#2• Therapy: dialysis=70%

– transplants=30%

• ESRD deaths: 50% cardiac causes. – 10-25% infectious

• Survival rates for 1,2,5 yrs= 79, 65, 34 % respectively

Pathophysiology of Uremia

• Excretory Failure: causes >70 chemicals to elevate. Urea= major breakdown of proteins. Limit protein intake

• Biosynthetic Failure: loss of hormones 1,25(OH)3 vit D3 and erythropoietin. – 85% of erythropoietin produced by kidney.– Vit. D3 deficiency= secondary

hyperparathyroidism, renal bone disease.

Pathophysiology of Uremia

• Regulatory Failure: over secretion of hormones , disruption of normal feedback mechanisms

Clinical Features of Uremia

• Neurologic complications:

• Subdural hematoma: 3.5% of ESRD, HTN, head trauma, bleeding dyscrasias, anticoagulants, ultrafiltration.

• Uremic Encephalopathy: nonspecific centreal neurologic symptoms, responds to dialysis.

• Neurologic complications: • Dialysis Dementia: like uremic

encephalopathy but progressive and fatal, seen after 2 years on dialysis

• Peripheral neuropathy: >50% of HD patients. “glove and stocking pattern”, improves after transplant

• Autonomic dysfunction: common; dizzy, impotence, bowel dysfunction.

• Cardiovascular complications: prevalence is greater in ESRD

• d/t pre-existing conditions, uremia, toxins, high lipids, homocystine, hyperparathyroidism, dialysis related conditions

• General population• CAD: 12%• LV hypert. 20%• CHF 5%

• ESRD• 40%• 75%• 40%

• Creatine protein Kinase &MB, Troponin I and T…….NOT significantly elevated in patients undergoing regular dialysis, have been shown to be specific markers in these patients.

• HTN: 80-90% of ESRD starting dialysis. d/t volume, vasopressor effects of kidney, RAS system. Tx initially w/ volume control

• CHF: HTN #1 cause in ESRD.

• Uremic cardiomyopathy: dx of exclusion when other causes of CHF ruled out.

• Pulmonary Edema: fluid overload, MI.– Tx w/ O2, nitrates, ACE inhib, morphine,

diuretics. Can also use phlebotomy, dialysis.

• Cardiac Tamponade: rarely w/ classic presentation of low BP, muffled sounds and JVD.– Echocardiography, pericardiocentisis

• Pericarditis/ Uremic Pericarditis:

• Uremic more common=75%

• Fluid overload, abnl platelet function, ↑ fibrinolytic and inflammatory cell activity

• Friction Rubs= louder, palpable, persist after metabolic abnormality resolved

• BUN always>60 mg/dl

• Absent EKG changes

• Dialysis related percarditis: recurrent, most common type during dialysis. More common adhesions and fluid loculations

• ESRD w/ pericarditis= 8%

• Tx w/ dialysis

• Avg survival without dialysis= 1 month

• Hematologic Complications:

• Anemia: low erythropoietin, blood loss from dialysis, ↓ RBC survival times– Normocytic, normochromic– Hct stabilizes @ 15-20 without tx.– Tx=erythropoietin

• Bleeding diathesis: ↑ risk of GI bleed, subdural.– Can try tx with desmopressin

• Immunologic deficiency: leukocyte chemotaxis and phagocytosis decreased in uremic state. – Dialysis does not help immune function.

• GI complications:

• Anorexia, nausea, vomiting=common in uremia

• Increased GI bleeding

• Chronic constipation

• Ascites from portal HTN, polycystic liver ds., fluid overload.

• Renal Bone Disease:

• Systemic calcification; ↓ GFR=↑ serum phosphate levels. – Pseudogout, metastatic calcification of

tissues, vessels. – Tx=low Ca dialysate and phosphate-binding

gels

• Hyperparathyroidism (Osteitis Fibrosa Cystica); – ↓ ionized Ca=↑ PTH= high bone turnover,

weak bones. – Tx=phosphate binding gels, Vit D3

replacement, subtotal parathyroidectomy

• Osteomalacia; defect in bone calcification

• d/t Vit.D3 deficiency and aluminum intoxication

• Weakened bones, muscle pains, weakness

• Low PTH, ow to normal alkaline phosphate levels, ↑ serum aluminum

• Tx= desferrioxamine

• Β2-Microglobulin amyloidosis:

• Pts >50 yrs old, on dialysis >10 yrs

• Amyloid deposits in GI tract, bones, joints.

• Complications; GI perfs, bone fx’s, carpal tunnel, rotator cuff tears.

• Pts w/ amyloidosis have ↑ mortality rates

Hemodialysis

• Uses ultrafiltration and clearance to replace nephron.

• Solute removal depends on filter pore size and concentration gradient

• Heparin 1000-2000 units typically used

• Sessions take @ 3-4 hrs.

Vascular Access Complications

• Types of Access:

• 1. A-V fistula

• 2. Vascular graft: higher complication rates, shorter functional lifes.

• 3. Tunnel-cuffed catheters; Hickman, Quinton

• Thrombosis and Stenosis of Access:

• Most common complication

• Loss of bruit and thrill

• Stenosis / thrombosis: not Emergencies= tx w/in 24 hours.

• Vascular Access Infections:

• 2-5% of fistulas, 10% of grafts

• Often signs of sepsis, fever, Hypotension, ↑ WBC

• Erythema, swelling, discharge at site often missing.

• Staph Aureus #1, gram neg #2

• Vanc is drug of choice, usually add Gent.

• Hemorrhage:

• d/t aneurysm, anastomosis rupture or over anticoagulation.

• Direct pressure

• Protamine 10-20 mg or 0.01 mg/unit hep.

• Consult surgery or nephrology

• Vascular access aneurysms:

• Repeated punctures

• Bulging in wall

• Rarely rupture

• True aneurysms very rare; 4% of fistulas

• Vascular access pseudoaneurysm:

• Subcutaneous extravasation of blood

• Present w/ bleeding & infection at site

• Vascular insufficiency: distal to access

• “steal syndrome”

• Preferential shunting of blood to low pressure venous side

• s/s exercise pain, non-healing ulcers, cool pulseless digits

• Dx w/ doppler or angiography

• High-output heart failure:

• When 20% of cardiac output diverted through access

• Branham sign: drop in HR after temporary access occlusion

• Doppler to measure access flow rate

• Surgical banding of access is Tx.

Complications During Hemodialysis

• 1. Hypotension:

• Most frequent, 10-20% of treatments

• Dialysis can remove up to 2 L/hr.

• Cardiac compensation limited d/t ↓ diastolic function common in ESRD

• Abnormalities in vascular tone; sepsis, anit HTN meds, ↑ nitric oxide

• Early hypotension: pre-existing hypovolemia

• Peridialysis losses; starts HD below dry weight; d/t sepsis, GI bleed, vomiting, diarrhea, decreased salt/water intake

• Intradialytic blood loss from tubing/dialyzer leads

• Hypotension at end of dialysis: excessive removal, cardiac or pericardial disease.

• Intradialytic hypotension:

• N/V/anxiety, ortho hypotension, tachycardia, dizzy, syncope.

• Tx.; stop HD, Trendelenburg. Salt, broth by mouth, NS 100-200 cc. IV.

• If these fail look for other causes than excessive fluid removal

• 2. Dialysis disequilibrium:

• End of dialysis

• N/V, HTN...progress to coma, seizure and death

• d/t cerebral edema after large solute clearance in HD

• Tx. Stop HD, administer Mannitol IV.

• 3. Air Embolism:

• s/s: dyspnea, chest tightness, unconscious, full cardiac arrest. Cyanosis, churning sound in heart from bubbles

• Clamp venous blood line, place supine

• Other Tx’s: percutaneous aspiration from R ventricle, IV steroids, full heparinization, hyperbaric O2 treatment

• 4. Electrolyte abnormalities:

• ↑ Ca, ↑Mg

• N/V, HA, burning skin, weakness, lethargy HTN

• 5. Hypoglycemia

Evaluation of HD Patients

• Dialysis schedule

• Dry weight

• Length of dialysis

• Inspect access site; erythema, swelling, tender, discharge.

• Peripheral edema, HJR, JVD not always CHF

• Murmurs; high flow d/t anemia?

Peritoneal Dialysis

• Peritoneal membrane= blood-dialysate interface

• Can be done acutely, chronically(continuous)=4 times/day, or multiple exchanges at night while sleeping.

Complications

• Peritonitis #1

• Mortality 2.5-12.5 %

• Fever, abd pain, rebound tender

• Dialysate fluid for cell count, Gram stain, culture

• Staph epidermidis 40%, S. aureus 10%, Strep species 15-20%, gram neg bacteria 15-20%, anaerobic bacteria 5%, fungi 5%.

• Empiric antibiotic therapy• Add to dialysate• Parenteral administration not needed• Rapid exchanges of fluid lavage to wash

out inflammatory cells• First gen Ceph• Vanc if pen allergic• Can add Gent

• Infections around PD catheter site:

• Pain, erythema, swelling, discharge.

• S. aureus, Pseudomonas aeruginosa

• Empiric w/ first generation Ceph or Cipro

• Outpatient therapy with f/u at CAPD center next day

• Abdominal wall hernia

• 10-15%

• Highest rate of incarcerating

• Immediate surgical repair

Overview Evaluating PD Patient

• Type and frequency of dialysis

• Date of last episode of peritonitis

• Frequency of relapse infections

• Baseline weight

• Focus on abdomen and catheter tunnel

Questions:

• 1. T/F Peripheral Neuropathy, “stocking and glove pattern”, is rarely seen in ESRD pts on dialysis.

• 2. T/F ESRD patients carry the same cardiovascular risk as general population.

• 3. T/F Troponins are commonly significantly elevated in patients on regular dialysis and cannot be trusted as cardiac marker.

• 4. #1 cause of dialysis access site infections…– A. klebsiella– B. staph aureus– C. strep species– D. E. coli

• 5. #1 complication during dialysis sessions is ….– A. hypotension– B. fever– C. CHF– D. cough

Answers: false (seen in 50%), false(inc risk), false, B, A.