module 10 Urogenital Emergencies Flashcards
Describe the physiology of potassium homeostasis
Potassium is body’s major intracellular cation and is key in the repolarisation of electrically active cells and return of the cell membrane to its normal resting potential. Potassium homeostasis relies on a balance between intake and excretion – there are no body stores.
RENAL;Potassium is freely filtered by the glomerulus; reabsorption occurs throughout the nephron, approx 1% is usually excreted.If there is hyperkalaemia potassium is still reabsorbed in the proximal tube and Loop of Henle, but secreted in both the distal tube and collecting duct, under the influence of aldosterone.
INSULIN;Activates Na+/K+ ATPase pumps in all cells
This moves sodium extracellularly and potassium moves intracellularly - resulting in increased intracellular potassium and a decrease in serum potassium.
ALDOSTERONE;Release stimulated by Angiotensin II, hyperkalaemia, ACTH and increased circulating catecholamines.
Increases Na+/K+ ATPase pumps in the basolateral membrane of cells in the distal collecting tubules. This increases sodium reabsorption and therefore water reabsorption.
Increases the number of potassium channels in the apical/luminal border of distal collecting tubular cells which facilitates the diffusion of potassium into the filtrate - and results in increased potassium excretion.
ADRENALIN;Beta2-agonists activity stimulates Na+/K+ ATPase pump
Stimulates insulin release
Alpha2-agonists inhibit insulin release
HOW ACID/BASE AFFECTS K+;
Metabolic acidosis results in increased serum potassium as decreased renal potassium excretion (potassium is exchanged for hydrogen movement into filtrate) & movement of hydrogen into cells in exchange for potassium.
Metabolic alkalosis results in decreased serum potassium due to K+movement into cells in exchange for hydrogen ions
OSMOLOALITY;Acute increases in serum osmolality results in water movement out of cells
This results in an increased intracellular potassium concentration and therefore increased gradient for the movement of potassium extracellularly into the serum. Every 10 mOsmol increase in osmolality of serum, potassium concentration of serum increases by 0.4 – 0.8 mmol/L
Discuss the aetiology, clinical consequences and management of hyperkalaemia
CAUSES OF HYPERKALAEMIA;
1. Increased intake (rare if kidney function normal).
2.Decreased excretion (most common). eg renal issue, urinary blockage, hypoA, d+, drugs eg ace inhibitor, spironolactone.
3.Redistribution; eg massive cell lysis, insulin deficiency or acidaemia (potassium leaves cells).
CLIN SIGNS;Hyperkalaemia results in a less negative resting membrane potential.
The cell membrane is more excitable but the cell can only generate weak action potentials. Eventually the resting potential becomes more positive and reaches the threshold potential and no action potential can be generated.
Generalised muscle weakness
Bradycardia – often inappropriate for clinical presentation - alarm bells
ECG abnormalities
Narrowed or spiked T waves
Prolonged PR interval
Shortened QT interval
Loss of P waves progressing to atrial standstill
Widened QRS progressing to sine wave formation
Cardiac arrest.
TX OF HYPERKALAEMIA;indicated if there are ECG abnormalities or neuromuscular weakness. When cardiotoxicity, treatment should be aggressive.
1. Cease any potassium supplements.
2.Fluid therapy is required to correct hypovolaemia and gfr. Any fluid will dilute potassium, may when faced with acidosis, select an alkalanising fluid.
3.10% calcium gluconate 0.5-1.5 mls/kg slow IV administration, over 5-20 minutes. Discontinue if bradycardia worsens. Effect lasts 0-45min. Does not alter potassium level, resets threshold of ap. May cause hypotension and bradycardia.
4. 50% dextrose 0.5-1ml/kg diluted 1:4 and given slow IV. This stimulates endogenous insulin release which moves potassium into cells.
5. Exogenous insulin administration (short acting/regular insulin) 0.25 – 0.5 IU/kg IV.Requires simultaneous glucose supplementation to prevent hypoglycaemia – 2g of 50% dextrose / Unit of insulin (4mls of 50% dextrose per Unit of Insulin)Must monitor glucose until can maintain normoglycaemia without supplementation (8-24hours)
6. Beta2-agonists eg.Terbutaline 0.01-0.02mg/kg slow IV for cats and dogs.Stimulates Na+/K+ ATPase and the intracellular movement of potassium. Onset of action in 30 minutes, effects last for up to 2 hours.Variable effect
7. Loop diuretics .eg furosemid.rarely used. Will promote some potassium excretion but worsens hypovolaemia.
8.Bicarbonate therapy. Rarely used due to side effects (increased carbon dioxide and sudden death)
9.Renal replacement therapy
Haemodialysis
Peritoneal Dialysis
Discuss the aetiology, diagnosis and management of uroabdomen
CAUSES OF UROABDOMEN;
1. Trauma eg blunt may rupture full bladder, pelvic fx may lacerate bladder or urethra, fx of spine or caudal ribs may lacerate kidneys, surgery or urethral catheterization.
2. Blocked urethra may cause bladder rupture
3. Neoplasia
Uroabdomen leads to hyperkalaemia, which stimulates aldosterone which leads to renal excretion of potassium which ends up in the abdomen instead, and hyperkalaemia causes heart issues….
DIAGNOSIS; clin signs vary depending upon duration. may have no signs to moribund. Urine in abdomen is highly irritant and causes peritonitis. If had uti prior to rupture, can have septic peritonitis. An intact-appearing bladder does not rule out uroabdomen from tear somewhere. Usually have metabolic acidosis, hyperkalaemia and azotaemia.
U/s find free fluid in abdomen. Must analyse the peritoneal effusion, which may be transudate, modified transudate or exudate.As irritant, usually have neutrophils >5000cells per uL, sG usually>1.025.
Compare peritoneal fluid with blood:
Glucose – glucose level 1.1mmol or more below blood glucose is highly specific for septic peritonitis.
Potassium concentration in effusion:blood >1.4:1 is highly sensitive and specific for uroabdomen.
Creatinine concentration in effusion:blood > 2:1 is 100% specific and sensitive for uroabdomen.
As well as u/s, may need xray and special contrast studies, and /or ct or mri.
MANAGEMENT;
1. Correct acid/base, electrolytes
2.If any concern re uti, start ab’s immediately else will become septic
3.Drain the abdomen and then ideally peritoneal dialysis
4. small tear in bladder might close if keep in dwelling urinary catheter in for a bit, otherwise surgery when stable. If urethral tear, place urinary catheter and refer. If ureteral or kidney tear, refer.
Discuss the aetiology, diagnosis and management of Feline Lower Urinary Tract
Disease (FLUTD)
AETIOLOGY; more common in male, overweight
desexed, less active, less water intake.
Possible causes:urethral plug or calculi, stricture, stress, neoplasia. Results in acute renal issues and hyperkalaemia.
DX; may have small bladder if irritated and voiding, may have large inexpressible bladder if blocked. Check for azotaemia and K+, xray/u/s, urinalysis, tp, pcv.
MANAGEMENT;
1. Analgesia eg morphine 0.3mg/kg i/m or sc q 4 hours. Or fentanyl CRI or buprenorphine 0.03mg/kg q 8hours.
2. Fluids.Used to treat hypovolaemia, hyperkalaemia and ongoing fluid requirements, as appropriate. More likely acidotic, so ) 0.9%NaCl whilst great for hyperkalaemia is a fraction acidifying so these days less favoured. Usually use buffered crystalloids even if contain small amounts of K+. Remember that post-obstructive diuresis can be as much as 25ml/kg/hour and occurs due to accumulation of osmotically active substances.
correction of severe hyperkalaemia as req.
3.Cystocentesis; risk of uroabdomen is considered low if done once. Recommend if do, that do with u/s guidance, with cat in dorsal recumbency, and go via right to avoid colon. Also recommend if do, that do a complete a drainage as possible. use samples for analysis and c+s. Reduces pressure on urethra and allows for gfr to recover. Also buys time if needed.
4. Catheterization;should be a completely sterile procedure. Any flushing should be done with sterile normal saline or sterile lube. Tom cat catheters of polypropelline are not for in-dwelling use and are more irritant. Use slippery sam (has stylet) or red rubber. Once in, flush bladder until is clear and no clots. Closed urine colection system recommended to help prevent against ascending infection and better monitor urine output. In-dwelling urinary catheters remain for 24-48 hours and are removed when urine is clear, azotaemia resolved, post obstructive diuresis resolved, and electrolyte disturbances resolved. Ab’s are NOT routinely used, and are only used if evidence of pre-existing infection (everything should have been sterile). Smooth muscle relaxants of arguable benefit. Ensure urination post catheter r/o.
Describe the pathophysiology of acute kidney injury and the differential diagnoses for
pre-renal, renal and post-renal causes
PATHOPHYSIOLOGY;Normal urine production for dogs is 1-2mls/kg/hr, cats is 1-1.5mls/kg/hr.Oliguria=insufficient urine production and is <0.25-0.5mls/kg/hr, or if on i/v fluids, urine output 0.5-1ml/kg/hr is suggestive of oliguria. (Oliguria is also ddx pre renal, renal or post renal)
Anuria=<0.25mls/kg/hr.
Decreased effective renal perfusion leads to ATP depletion, causing cytoskeletal changes in renal tubular epithelial cells. Decreased GFR results in persistent injury and release of inflammatory mediators and interactions between epithelial and endothelial cells. Apoptosis and acute tubular necrosis results. Formation of urinary casts secondary to tubular necrosis can block the nephron leading to further damage. Whether kidneys can recovery, depends on length of insult and balance between injury and healing.
(Proteinuria ddx damage to glomerular membrane or presence of inflammation).
DDX PRE RENAL;
Decreased GFR - hypovolaemia, hypotension or excessive vasoconstriction
Systemic disease - SIRS, DIC, sepsis, etc
NSAIDs - block autoregulation of renal BP
DDX RENAL; (renal issue or anything cause pre renal or post renal azotaemia can also result in renal injury)
Vascular disease
Embolism
Glomerular disease
Immune mediated
Inflammatory - can decrease GFR or make the glomerulus more permeable to proteins etc
Tubular disease
Toxins / drugs - numerous
NSAIDs - overdose, inappropriate use (e.g. owner giving when not safe or using ibuprofen etc), adverse drug reactions
NSAIDs block cyclooxygenase reducing prostaglandin synthesis and therefore disrupt auto-regulation of renal blood supply in low flow states
Grapes, lilies (MOA unknown)
Ethylene glycol, heavy metals
Penicillins can cause direct tubular injury and are also eliminated by kidneys, aminoglycosides.
Ischaemia
Hypercalcaemia - >3.7 mmol/L causes renal vasoconstriction and decreased GFR
Interstitial disease
Pyelonephritis
DDX POST RENAL;
Urinary tract rupture
Urinary tract blockage - urethral or bilateral ureteral (bilateral), bladder neoplasia
Prostatic disease
List the veterinary staging systems for acute kidney injury
IRIS (International Renal Interest Society) Scheme for Acute Kidney Injury;
Grade I:
Documented AKI (history, clinical, laboratory or imaging evidence)
Oliguria or anuria which is volume responsive (increases to >1ml/kg/hr over 6 hours with fluids)
And/or progressive non-azotaemia increases in blood creatinine > 26.4umol/L (but <140umol/L) during a 48h interval
Grade II:
Documented AKI and static or progressive azotaemia
Creatinine 141-220umol/L (or progressive increases > 26.4umol/L over 48 hours)
Azotaemia is volume responsive (decreases to baseline over 48 hours)
Documented oliguria that is responsive to fluid
Grade III
Moderate to severe documented AKI
Creatinine 221-439 umol/L
Grade IV
Moderate to severe documented AKI
Creatinine 440-880 umol/L
Grade V
Moderate to severe documented AKI
Creatinine >880 umol/L
Discuss the treatment, management and monitoring of acute renal injury
Treat early, and treat underlying cause (eg ab’s for pyelonephritis). repeated testing is necessary.
1. Discontinue any nephrotoxins.
1b. TREAT UNDERLYING CAUSE
2. Fluids /electrolytes as required. Colloids likely detrimental for acute renal injury.
Hyperkalaemia - common in oliguria and post renal AKI
Improves once urinary flow is re-established
May require specific treatment if cardiotoxicity occurs (see above)
Hypokalaemia- may develop with polyuria and inability to concentrate urine
Supplement as required
Hypernatraemia - occurs with dehydration and hypotonic fluid loss such as with vomiting
Hypochloridaemia - chloride loss occurs with vomiting
Hypocalcaemia - wasting due to polyuria
Can be associated with clinical signs and should be supplemented with the minimally effective dose of calcium gluconate
Hypercalcaemia – due to decreased GFR and therefore reduced excretion
Standard fluid parameters of boluses to correct hypotension, then fluid losses and dehydration management, then ongoing losses.
Attempting to induce diuresis(increased urination) is detrimental as it leads to fluid overload. Fluid overload leads to interstitial oedema and poor outcome.
If overload occurs fluids should be stopped completely
If the patient is rehydrated and anuric then only enough fluid should be given to replace insensible losses (12-29ml/kg/day).
Be aware that during recovery, oliguria may become polyuria. Monitor ins and outs and patient status.
3.Diuretics generally frowned upon as worsen kidney injury. Rarely, in oliguria/anuria may be used where the goal is to be able to manage minimum fluid requirements without resulting in fluid overload.
4. Manage nausea
Antiemetics
maropitant
metoclopramide - care regarding dose as is excreted by kidneys
H2 blockers
ranitidine 1-2mg/kg IV q12hrs (has questionable efficacy in dogs)
GI ulceration can occur in AKI likely related to stress induced mucosal disease
may accumulate if there is decreased renal function
Proton pump inhibitors
e.g. esomeprazole 1-2mg/kg q 12-24 hrs
5. Renal transplant for patients with inadequade renal function to manage uraemia and acid/base/electrolyte disturbances.
Discuss the diagnosis and treatment of pyometra
DIAGNOSIS;xrays, mucopurulent vaginal discharge (open), u/s.
note average age dog os 8-9 years whereas average age cat is 2.5 years.
TREATMENT;
1. Surgery-ideal. esp for sepsis, ruptured uterus, closed, intrauterine foetus and very ill. 24-48 hour monitoring post op recommended.Complications include Peritonitis (most common),Anorexia,Pyrexia,Vomiting, Renal insufficiency.
2. Medical; eg for young healthy breeding animals or if surgery/anaesthesia is dangerous.BUT must revert to surgery if not responding to medical management.Remove the effect of progesterone to allow cervical relaxation, myometrial contraction and improve uterine immunity – Dinoprost 20 mcg/kg IM q8h for up to 8 days or 30 mcg/kg SC q12h for 8 days
Prevent bacterial proliferation – Amoxycillin-clavulanate 12.5-20mg/kg q8-12h SC/IV/PO
Increase vaginal discharge is seen within 24-36 hours and last for 7-10 days
Breeding in the next oestrus cycle is recommended
Discuss the diagnosis and treatment of eclampsia
Eclampsia is an acute, potentially life-threatening condition in the periparturient period due to hypocalcaemia. It can be caused by several factors including poor maternal diet during pregnancy, parathyroid gland disorder (acquired or iatrogenic e.g. excessive calcium supplementation) and systemic illnesses that cause hyporexia in late gestation and early lactation.
SIGNALMENT;
Within 4 weeks of the start of lactation – typical
Can occur in late gestation or at any time during lactation
Small breed dog with a large litter – typical
Can be seen with any breed dog with any litter size
CLIN SIGNS;
Muscle fasciculations, hypertonicity
Seizures
Ataxia, dysmetria
Stiff gait
Hyperthermia/pyrexia
Pruritus
DX;Might see;CBC – non-regenerative anaemia (common in late gestation)
Biochemistry – hypomagnesaemia, hypo or hyper phosphataemia and hypoproteinaemia, hyperkalaemia. Total calcium maybe normal or reduced.WILL have low ionized calcium. REMEMBER that most machines are measuring total calcium.(ie still tx with calcium when the clinical signs fit even if total calcium normal).
TX;
10% calcium gluconate at 0.5 to 1.5ml/kg over 10-30 minutes
* Must monitor ECG for signs of arrhythmias/bradycardia and vomiting. Stop immediately. Once ECG have normalised, infusion can be resumed at a slower rate.
Diazepam 0.5mg/kg IV to control seizure
Supportive treatment for:
Hypoglycaemia – 0.5g/kg glucose (1ml/kg of 50% glucose, diluted 1:4) IV
Hyperthermia – active cooling
Cerebral oedema – Mannitol 0.25g/kg IV slow or 7% HTS at 3ml/kg over 15-30 minutes.
Then ongoing management is Oral calcium supplementation at 25-50 mg/kg/d elemental calcium and
remove neonates from the dam.
Discuss the recognition and management of dystocia
Dystocia is a difficulty in passing foetus through the pelvic canal.
NORMAL PARTURITION;
Stage 1 – Indiscernible uterine contraction and progressive cervical dilation
Behavioural change – nesting, panting and restlessness in the bitch; vocalisation, rapid breathing, restlessness and loud purring in the queen
Lasts 6-12 hours
Stage 2 – Foetal expulsion through the fully dilated cervix
Visible abdominal straining that matches strong uterine contractions
Bitch
first foetus delivered within 30 minutes of the start of stage 2 labour
should be complete within 12-24 hours
foetus is produced every 30 minutes to 1 hour
Queen
can last for up to 42 hours
foetus produced every 4 hours
Stage 3 – Expulsion of placenta
5-15 minutes after delivery of foetus
Multiple can be passed after several puppies are delivered close together
DYSTOCIA;
Dystocia of maternal origin – 60-70% cases
Primary uterine inertia – most common
Complete or partial
Failure of uterus to contract in an organised manner
Can be due to the size of the litter – too small or too large
Can be due to inherited predisposition, age related changes, systemic disease, nervous inhibition, nutritional or neuroendocrine abnormality
Secondary uterine inertia
Can occur due to anatomical or physiological cause
Exhaustion of uterine musculature after contracting against an obstruction or due to delivery of a large litter
Potential causes are narrow pelvis, congenital malformation of the pelvis, pelvic trauma, neoplasia, vaginal stricture, uterine torsion, uterine or vaginal prolapse
Dystocia of foetal origin
Malpresentation – most common
Cephalopelvic disproportion
Foetal anasarca
Foetal oversize
Foetal death
QUALIFIES AS DYSTOCIA if;
Prolonged gestation >72 days in the bitch and >71 days in the queen
Failure to deliver foetus >24 hours after onset of stage 1 labour
Green discharge prior to delivery of first foetus
Strong, active abdominal contraction for 30 mins without expulsion of a puppy
Greater than 3 hours since delivery of the last foetus
Stage 2 labour lasting >24 hours in the bitch and >42 hours in the queen
Membranes or part of foetus protruding >15 mins without delivery of foetus
Signs of systemic illness in the dam
TREATMENT OF DYSTOCIA;
Medical management should only be attempted if the dam is healthy, the cervix is dilated, foetal size and positioning is suitable for vaginal delivery and foetal heart rate is normal.
1.Medical management
Obtain radiograph to rule out potential obstruction
Perform abdominal ultrasound to obtain foetal heart rate
Foetal heart rate <180 bpm indicates foetal stress and hypoxia
Foetal heart rate <160 bpm indicates the need for immediate surgical intervention
Sterile vaginal examination and attempt at digital manipulation of foetus if required
Oxytocin 0.1 U/kg IM or SC q30 mins, no more than 2 doses due to the risk of uterine hyperstimulation or foetal distress associated with placental separation
Calcium (0.5ml/kg 10% calcium gluconate IV slow) can be used in addition to Oxytocin if calcium is low
Glucose supplementation if required
2.Surgical intervention
Caesarean is required in 60% of cases of dystocia.
Criteria for caesarean:
Complete primary uterine inertia
Partial primary uterine inertia not responsive to medical management
Secondary uterine inertia
Obstructive abnormality of the pelvic canal
Foetal malposition that cannot be corrected
Foetal death
Relative or absolute foetal oversize
Foetal distress
ideally NO premed, if patient difficult to handle, recommend methadone 0.4mg/kg IM with o holding head and yes add in some acp if very obnoxious. Neonates might need several doses of naloxone after methadone though. I/m alfaxon is arguably worse for neonates and cannot reverse it.
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