Urinary system & renal emergencies Flashcards
In oliguric renal failure, what is the main goal of therapy and what diuretic strategy is used?
To increase urine production, reduce tubular obstruction and increase kaliuresis.
Osmotic and loop diuretics i.e. frusemide and mannitol (after rehydration) are used.
Urosepsis
Sepsis associated with a complicated UTI (bacterial pyelopnephritis, pyonephrosis, renal abscess, fungal infection, bladder perforation, prostatic/testicular infections)
Most common uropathogen
E. coli (<50% of all cases)
Local host defense mechanisms preventing ascending UTI
Normal microturition
Extensive renal blood flow
Normal urinary tract anatomy
Urethral and uteral peristalsis
Mucosal defense
Antimicrobial properties of urine
Systemic immunocompetence
Risk factors for UTI
Abnormal urinary anatomy
Urinary obstruction
Nephrolithiasis
Prior UTI
Renal failure
Neurologic disease
DM
Hyperadrenocorticism
Immunosuppresion
Clinical and lab findings in urosepsis patients
lethargy
fever of hypothermia
hyperaemic MM
tachycardia
tachypnoea
bounding pulses
positive blood culture
leukogram (+- left shift)
Azotaemia
Urine sediment
MODS (and signs of MODS)
Aggressive treatment of urosepsis
IVFT
Broad-spectrum antimicrobials
Addressing the underlying cause
Pyelonephritis
The kidneys and ureters are affected most commonly by ascending bacteria
Signs of pyelonephritis
Febrile
Anorexia
Lethargy
Dehydration
Recent weight loss
Enlarged and painful kidneys
PU/PD
Vomiting
Lab and imaging findings with pyelonephritis
Azotaemia
Neutrophilic leukocytosis with left shift
Metabolic acidosis
mild to moderate pelvic and ureteral dilation
Poorly concentrating urine
Bacteriuria
Pyuria
Proteinuria
Haematuria
+- granular casts
Treatment of pyelonephritis
Removal predisposing factors
IVFT
Broad-spectrum antimicrobials (4-8 weeks)
Urine C&S
Nephrectomy
Ureteral stent
Bladder rupture
Usually occurs after blunt force trauma, penetrating injuries, aggressive catheterisation, prolonged urethral obstruction or excessive force when palpating the bladder.
Signs of bladder rupture
Vomiting
Anorexia
Depression
Abdominal pain
Systemic inflammation
Diagnosis of uroabdomen/uroperitoneum
Comparing abdominal fluid to peripheral blood creatinine and/or potassium ratios. A fluid to serum potassium ratio > 1.4 to 1 has 100% sensitivity and specificity for uroabdomen. A fluid to serum creatinine ratio > 2 to 1 has a 100% specificity and 86% sensitivity
Prostatic infection
bacterial colonisation via ascension of urethral flora or hematogenous route.
Clinical signs of prostatic infection
Anorexia & weight loss
Vomiting
Tenesmus & rectal pain
Lethargy
Fever
Dehydration
Injected MM
Caudal abdominal discomforrt
Haematuria
Pyuria
Stranguria/incontinence
Lab findings of prostatic infection
Mature neutrophilia and evidence of left shift
Septicaemia
Endotoxaemia
Inflammatory changes in prostatic fluid
Imaging findings of prostatic infection
Prostatomegaly
Localised peritonitis
Cyst like structures
Treatment of suppurative prostatitis and prostatic abscessation
IVFT
Treat cardiovascular shock
Antimicrobial therapy
The RAAS system works to:
a. increase perfusion to the kidneys
b. decrease blood pressure
c. increase sodium excretion
d. decrease serum potassium levels
A
Which of the following is an example of intrinsic kidney injury?
a. Hypovolemic shock
b. Urinary obstruction
c. Grape toxicity
d. Ureteroliths
C
Sodium bicarbonate, insulin, and beta-2 adrenergic agonists can all be administered to treat:
a. azotemia
b. hyperkalemia
c. oliguria
d. stage 2 AKI
B
Which of the following antibiotics is an acute renal toxin?
a. Amikacin
b. Metronidazole
c. Penicillin
d. Cefazolin
A
In veterinary acute kidney injury staging, stage 3 patients have a:
a. creatinine increase of <100% from baseline
b. creatinine increase of 150–199% from baseline
c. creatinine increase of 200–299% from baseline
d. creatinine increase of >300% from baseline
D
When performing peritoneal dialysis, dextrose concentrations of 2.5% are used in which patients?
a. Normovolemic
b. Dehydrated
c. Mildly overhydrated
d. Severely overhydrated
C
Glucose is reabsorbed in which section of the nephron?
a. Proximal convoluted tubule
b. Loop of Henle
c. Distal convoluted tubule
d. Collecting duct.
A
Which of the following is not nephrotoxic in dogs?
a. Ethylene glycol
b. Xylitol
c. Raisins
d. Ibuprofen
B
Which of the following is not a cause of postrenal azotemia?
a. Urethral obstruction
b. Prostatic disease
c. Ureteroliths
d. Hypovolemic shock
D
patient producing 0.4^mL/kg/h of urine would be classified as what level of urine output?
a. Anuric
b. Oliguric
c. Normal
d. Diuresis
B
Which of the following diseases is best treated with intermittent hemodialysis over CRRT?
a. Ethylene glycol toxicity
b. AKI
c. Heat stroke
d. Chronic kidney disease
D
Which of the following patients may need packed red blood cells to prime the CRRT pump?
a. A cat with lily toxicity
b. A Labrador with AKI
c. A husky with ibuprofen toxicity
d. A rottweiler with sepsis
A
A patient suffering from AKI and fluid overload would benefit from which of the following treatments?
a. Continuous venovenous hemodialysis
b. IV fluids prior to CRRT
c. Slow continuous ultrafiltration
d. Continuous venovenous hemofiltration
C
Which of the following drugs is renal replacement therapy not an ideal treatment for?
a. Amikacin
b. Bupivacaine
c. Phenobarbital
d. Sotalol
B
Diffusion is defined as which of the following?
a. Movement of solutes from a higher concentration to a lower concentration
b. Movement of fluid through a semi-permeable membrane via a pressure gradient
c. Movement of solutes with water flow
d. Adhesion of molecules from a liquid to a solid surface
A
Which of the following is a complication of CRRT?
a. Hyperthermia
b. Hypertension
c. Hyperkalemia
d. Hemodilution
D
A complication of dialysis that stems from the development of cerebral edema due to rapid changes in osmolality of the blood is called what?
a. Cerebral ischemia
b. Dialysis disequilibrium
c. Azotemia
d. Hyperelectrolytism
B
Why is anticoagulant therapy a mainstay of hemodialysis treatment?
a. To thin the blood to go through the dialysis catheter
b. To prevent clot formation in the extracorporeal circuit
c. To balance the thrombus-inducing effects of the dialysate
d. To maintain a state of homeostasis
B
Which of the following toxins is most likely to warrant treatment with dialysis?
a. Xylitol
b. Zinc
c. Ethylene glycol
d. THC
C
Which molecule would not be found in a dialysate?
a. Dextrose
b. Sodium
c. Chloride
d. Albumin
D
Kidney function
Maintain homeostasis by blood filtration, reabsorption and excretion
What regulates the excretion & retention of water?
Antidiuretic hormone (ADH) released from the pituitary gland
Normal kidney size
2.5-3X larger than L2
Kidney location
Retroperitoneal cavity
Nephron
Basic functional unit of the kidney
Cats: 190,000
Dogs: 415,000
Renal corpuscle
Filters the blood in the first stage of urine production, producing glomerular filtrate
PCT
resorptive and secretory functions producing primitive urine. Glomerular filtrate -> tubular filtrate.
Reabsorbs 50-55% filtrated water, phosphorus, glucose and sodium.
L.O.H
electrolyte exchange, absorption & secretion
Absorbs Na, Cl, Ca, Mg but is impermeable to water making filtrate hypo-osmolar.
DCT
Empties tubular filtrate into a series of collecting ducts into the renal pelvis and onto the ureter.
Sodium & chloride further absorbed but NO absorption of water.
Sensitive to parathyroid hormone (regulates Ca reabsorption)
Collecting ducts
Determines urine volume as this is the primary acting site of ADH, regulates K and plays a role in acid-base.
Fluid hypo-osmolar approx. 100mOsm/kg
How much blood supply from the heart does the kidney receive?
25%
Renal artery
Comes from the abdominal aorta entering the hilus of the kidney and further subdividing into smaller arteries & arterioles (afferent & efferent)
Afferent glomerular arterioles
Carry blood to the glomerular capillaries of the renal corpuscle
Efferent glomerular arterioles
surround the nephron and transfer oxygen to the cells
Renal vein
Leaves the kidney hilus and joins the abdominal portion of the vena cava (purest blood in the body)
Mean renal arterial pressure and glomerular capillary pressure
100mmHg & 50-55mmHg
Filtration of blood
Occurs in the renal corpuscle
Glomerular filtration rate
How fast plasma is filtered as it passes through the glomerulus
Dogs 3-5ml/kg/min
Cats: 2.5-3.5ml/kg/min
Kidneys reabsorb _____ of plasma water
99%
Urine production is dependent on…
Renal blood flow and proper nephron function
Autoregulation
Describes the process where the kidney adjusts RBF by constricting and dilating the afferent & efferent arterioles in response to changes in MAP to maintain normal GFR.
* Becomes ineffective when MAP <60-70mmHg
* MAP 80-100mmHg allows kidney to maintain RBF & GFR than varies <10%
Why are the kidneys sensitive to damage?
Receive approx. 20-25% of CO and 90% of this being delivered to the kidney cortex. This means any damage decreases kidney perfusion, exposes nephrons to toxins from the blood and dysregulates autoregulation which can induce ischaemic injury.
Cut off for clinical signs of kidney injury
Clinical signs will only manifest after 66% of function lost and >75% loss of function is deemed renal failure
Azotaemia
Increase in BUN and Creatinine
Pre-renal azotaemia
“Before the kidney” and occurs due to decreased renal blood flow affecting GFR.
- hypovolaemia, hypotension, haemorrhage, third-spacing fluids
Instrinsic/renal azotaemia
Caused from damage to the cellular structure of the kidney or an ischaemic/toxic event
- nephrotoxicity, ischaemia, infectious agent
Post-renal azotaemia
“Below the kidney” Obstruction or diversion of outflow of urine
- FLUTD, bladder herniation, trauma
Dysuria
Difficult urination
Stranguria
slow, painful urination
Pollakiuria
Excessive frequency of small volume urination
Reflex dyssynergia
Decreased urine stream “spasm”
Periuria
Inappropriate urination
Incontinence
Involuntary urination
General signs of uraemia
Hypothermia
Dehydration
Depression
FLUTD
Inability of urine to flow from the body likely due to a uretheral plug of crystalline/mucous material forming a physical obstruction. Most common form of post-renal azotaemia in male cats.
Treatment of hyperkalaemia in FLUTD cats
- Cardiac protectant = CaGlu
- Dextrose
- Fluids
- Insulin
- Terbutaline
Common ECG finding in blocked male cats with hyperkalaemia
Sine wave
- diminised P wave with tall T wave, wide QRS
Best pain relief for cats suffering FLUTD
Pure mu opiod i.e. fentanyl, methadone
Common signs of FLUTD
- frequent trips to litter box
- excessive grooming of the urogenital area
- dehydration
- vomiting
- stranguria and/or pollakiuria
- vocalisation
- abdominal pain
Treatment of recurrent (>3) UO
Urethrostomy
VAKI staging for AKI
Stage 0: Crea inc. by <150%
Stage 1: Crea inc. by 150-199% or 0.3mg/dL
Stage 2: Crea inc. by 200-299%
Stage 3: Crea inc. by >300% or >4mg/dL
Four phases of AKI
- Initiation: insult occurs, unlikely to detect biochemical or cellular change
- Extension: insult has occurred, biochemical & cellular changes don’t show full extent of injury
- Maintenance: kidneys reach maximal damage
- Recovery: Start to see improvement in kidney function with treatment
Treatment for AKI
IVFT
Diuretics
Bicarbonate therapy (care)
Renal replacement therapy
Anti-emetics
PPI
Nutrition
Bicarbonate dose
0.3 X BW X BE
Give 1/3-1/2 of dose dilutes and then give remainder over 4-6h but monitor blood gas
Diagnostic for uroabdomen
Fluid to serum potassium >1.4 to 1
Fluid to serum creatinine >2 to 1
Fluid therapy in AKI
Aim for neutral fluid balance and avoid over hydration (optimise GFR, overload + <10% weight gain)
- monitor weight and ins and outs
Want to restore kidney perfusion and keep up with losses
Isotonic balanced crystalloid preferred
Diuretics in AKI
Furosemide and mannitol
Response to administration might be a favourable indicator of survival and tip fluid balance back to neutral
Poor response may mean no urine being produced
Insensible losses
12-29ml/kg/day
Acid-base changes in AKI
Likely metabolic acidosis as retention of H+ ions and poor reabsorption of HCO3
There may be a secondary lactic acidosis due to poor renal perfusion
Hyperkalaemia may require treatment
Elevated K in AKI
Excitatory cells are refractory to repolarisation leading to reduced conduction of cardiac and neuromuscular tissue.
- tent T
- wide QRS
- short QT
- sine wave
- small, wide or absent p waves
- atrial standstill
- ventricular fibrillation
Besides fluid therapy what are some other treatment strategies in AKI
Gastroprotectants
Anti-emetics
Nutritional support inc. phosphate binders
RRT
- when pulling back only reduce fluids by 10% a day
Clinical presentation of AKI
Anorexia
Dehydration
Weight loss
Listlessness
Oliguria/Anuria/ PU PD
Neurological signs
Oral ulceration
Enlarged, painful kidneys
Peripheral oedema
Bradycardia
Gastritis/eneteritis
Urinalysis findings in AKI
Crystals - calcium oxalate if ethylene glycol
Dipstick - proteinuria, billirubinuria, glucosuria, haemoglobinuria
Isosthenuria
Normally acidic (unless UTI)
Pyuria
C&S required
Imaging findings in AKI
Renomegaly
Liths
Perirenal fluid
Pelvic dilation/obstruction
Ethylene glycol hallmarks
Severe metabolic and lactic acidosis
Profoundly low iCa
Profoundly large anion gap
Low albumin
Severe hyperphosphotaemia
Azotaemia
Oliguria/Anuria
Calcium oxalate crystals
Bright kidneys
CKD patients
Have inflammatory infiltrates and degrees of fibrosis as well as tubular atrophy, glomerular sclerosis. Progression of CKD is due to ongoing insult which after a certain amount of damage is irreversible.
IRIS stages (creatinine)
Stage I <1.4; <1.6
Stage II 1.4-2; 1.6-2.8
Stage III 2.1-5.0; 2.8-5.0
Stage IV >5.0; >5
Clinical presentation of CKD
PU/PD
Dehydration
Seizures
Anorexia
Vomiting/Dysphagia
Halitosis
Pallor
Oral discomfort and ulceration
Weakness
Muscle atrophy
Heart murmur
Hypothermia
Diagnostic findings of CKD
Azotaemia
Metabolic acidosis
Increased phosphorus, potassium, CK, calcium
Hypertension
Chronic inflammation
Anaemia
Normal PLT # but reduced function
Hypoalbuminaemia
Sediment
UPC >2
Diminished renal architecture, mineralisation and abnormal shape/size
Low GFR
… more …
Treatment of CKD
Correct hydration
Treat acid-base and electrolytes
Manage GIT signs
Nutritional support: feeding tubes, appetite stimulants, restrict protein & phosphorus
Manage anaemia
Manage hypertension: amlodipine and ACE
Calcitriol (dogs)
Indications for renal transplant
Cats suffering irreversible AKI or CKD without underlying pathology and are otherwise well
If UTI present prior to renal transplantation
Cyclosporine trial for 2 weeks and should be negative after
Heart murmurs are ok for renal transplant patients
Yes as long as they are physiological I.e. anaemia or from CRF
Renal transplant donors
Generally 1-3 years old and in excellent health
Adopted by the family or failed donors rehomed
Must have prior screening and CT
Preoperative treatment for kidney transplantation
IVFT 1.5-2X maintenance
Haemodialysis (Crea >8 and BUN >100)
Amlodipine or hydralazine if hypertensive
Wole blood transfusion if anaemic
EPO if delayed transplantation aiming for PCV at least 30%
Feeding tubes if anoretic
Immunosuppressive 72-96h prior with cyclosporine
Anaesthetic management of kidney transplantation
Both donor and recipient receive cephalexin
Bupivicaine epidural to donor and recipient
CVC in recipient
Doppler BP
If hypotensive drop inhalants
Dopamine as required
Why is mannitol given during kidney transplantation
Increase RBF
Prevent renal artery spasms
Protect the kidney from injury
Postoperative care of renal transplantation
IVFT
Monitor weight, UOP, hydration closely
Minimise stress
Provide antibiotic 2-3 weeks after
Regulate CSA levels
Give clindamycin if positive for toxoplasma
Serial BP
2X daily full bloods until stable
Long term management for kidney transplantation
Follow ups initially weekly, then monthly, then biannually
Remove feeding tube once eating appropriately and tube has been in at least 7-10 days
Watch for rejection, thrombosis, CaOx, infection due to immunosuppressive agents and retroperitoneal fibrosis
Success of renal transplantation
70-93% and live between 360-616 days
IHD and CRRT
Renal replacement therapies that are instituted for patients with fluid overload and/or AKI. CRRT preferred in the ICU setting and haemodynamicslly unstable patients.
ECT basic mechanism
Blood removed from patient > treated/processed > blood returned to patient and effluent with toxins wasted
Peritoneal dialysis
Peritoneal surface utilised as the dialysis membrane and so mix in peritoneal space and diffuse until ‘equilibrium’ and then that fluid is removed
Approx. 30-40ml/kg exchanged per cycle
Indications for IHD or CRRT
Severe azotaemia despite traditional therapy (BUN >100mg/dL, crea >10mg/dL)
Refractory hyperkalaemia despite traditional therapy
Patient status deteriorating
Severe acid-bae abnormalities
Fluid overload
Uraemic toxaemia not responding to treatment
Preferred ECT therapy
IHD
Increased rate of solute removal of low molecular weight per unit of time
How long is CRRT continued
Until patient goals are met: stabilisation of azotaemia, stable acid-base, correction of fluid overload
- may require more than one treatment
Dialysis
Diffusion and convection across a semi-permeable membrane dependent on:
- solute size/MW/charge
- concentration gradient
- surface area
- permeability of membrane
What solutes easily dialyse and which don’t + cut off points
Freely diffuse: electrolytes, BUN ~60Da (<500Da low molecular weight)
Do not diffuse/diffuse with great difficulty: albumin ~66,400 Da
Medium molecular weight 500-60,000Da
Large molecular weight >60,000
Where is blood returned in dialysis
Right atrium
Preferred RRT for fluid overload
Ultrafiltration especially if Oliguria
Contraindications for RRT
Severe coagulopathy
Severe hypotension
Small patient size
Dialysis catheter anatomy
Proximal - arterial, blood drawn into unit
Distal - venous, blood returns to patient
- prevents recirculation
- locked with heparin after treatment
- for PD catheters there are acute (<3 days) and chronic (long term) types
Why do we avoid rapidly removing uraemic toxins
To avoid disequilibrium that results from too rapid change in osmolality resulting in neurological derangement and signs due to cerebral oedema
Ideal fluid removal rate in RRT
<10ml/kg/hr
Goals of RRT
Maintain fluid, electrolyte and acid-base
Prevent renal damage
Promote renal recovery & healing
IHD
Increased flow so that solute removal occurs more rapidly using diffusion principles
CRRT
Used for AKI, toxins, sepsis, heat stroke etc
Slower removal of toxins compared to IHD which may benefit haemodynamically unstable patients
Tries to mimic normal kidney function
Uses convection and diffusion principles
Generally removes low and medium molecular weight molecules, inflammatory mediators and toxins
Criteria for a toxin to be dialysable
Low volume of distribution (Vd)
Low protein binding
Low/medium molecular weight
Low exogenous clearance
Water soluble
Examples of dialysable toxins
Ethylene glycol
Aspirin
Acetaminophen
Theophylline
Barbiturates
Alcohols
Some antidepressants
Amikacin (+ some other AB’s)
B-blockers
Caffeine
Some chemotherapy agents
Gabapentin
Mannitol
Priming stage of CRRT
Usually performed with NaCl but consider colloids and blood products in smaller patients
Some blood volume removed (Hypovolaemia and anaemia may incur)
Priming prevents haemodilution and ensures adequate tissue perfusion
Remove air if in line
Dialysates
Mix of purified water and electrolytes and buffer
Can add additional electrolytes if needed to tailor to patient
Which part of the dialysis machine acts as the nephron
Haemofilter
Patient prep for RRT
Large bore, silicone or polyurethane catheter into the jugular - Place tip at junction of the cranial vena cava and R atrium (approx. 4th intercostal space)
Warm patient
Have other medical therapies inititiated
General flow rates of CRRT for cats and dogs
Cats <80-125ml/min
Dogs <250-1500ml/min
Where is the #1 site of bleeding visualised in a coagulopathic animal receiving ECT
Dialyser catheter site
Dialysis disequilibrium syndrome (DDS)
Directly related to the rate that dialysis is occuring
Massive osmolality change resulting in the development of cerebral oedema
Usually seen in the first few treatments in the first few hours particularly if very uraemic
Signs: agitation, vomiting, restlessness, seizures, coma, death
Potential complications of RRT
Hypotension
Anaemia
Coagulopathy
Hypothermia
Draw and explain the 4 dialysis modalities
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Anticoagulants in RRT
Given to prevent clot formation in the extracorporeal circuit that can cause significant anaemia and other problems
D/C approx 30min before end of treatment
Unfractioned heparin most common
Watch for bleeding and haemorrhage
Nursing considerations in RRT patients
Require 24h monitoring
Patient may require sedation
Watch for signs of bleeding
Serial BP monitoring (if low reduce flow right or consider IVF bolus)
Monitor temperature
Regular blood tests: VBG, electrolyte, coagulation profile
When to discontinue RRT
When desired effects achieved
- ensure rinse-back
- line flushed with NaCl and locked with heparin
