Urinary Flashcards
What is a UTI
Infection in the blasser causing cystitis and can soread to the kidneys causing pyelonephritis
More common in women where the urethra is much shorter making it easy for bacteria to get into the bladder
Main bacteria source is from faeces where the normal intestinal bacteria such as E.coli can easily make the short journey to the urethral opening from the anus
Sexual activity is a key method for spreading bacteria around the perineum and are also very common in women where incontinence or hygeine are a problem.
Urinary catheters are a key source of infection and catheter-associated UTIs tend to be more significant and difficult to treat
How do UTIs present
Lower urinary tract infections present with:
-Dysuria (pain, stinging or burning when passing urine)
-Suprapubic pain or discomfort
-Frequency
-Urgency
-Incontinence
-Confusion is commonly the only symptom in older more frail patients
Pyelonephritis presents with:
-Fever is a more prominent feature than lower urinary tract infections.
-Loin, suprapubic or back pain. This may be bilateral or unilateral.
-Looking and feeling generally unwell
-Vomiting
-Loss of appetite
-Haematuria
-Renal angle tenderness on examination
What are the significant findings on urine dipstick
Nitrites:
-gram neg bacteria (eg E.coli) breakdown nitrates (waste product in urine) into nitrites
-suggests bacteria presence
-better indication of infection than leukocytes
-If only N present, worth treating as a UTI
Leukocytes:
-WBC
-Normally small number of these in the urine but a significant rise can be the result of an infection or other cause of inflammation
-If only leukocytes, do not treat as UTI unless clinically evident UTI present
If both N and L present:
-treat as UTI
-Send to Lab for culture and sensitivity testing
If neither then unlikely to be UTI
What causes UTI
Most common: E.coli
-Gram neg
-Anaerobic
-Rod-shaped bacteria
-Part of normal intestinal microbiome
-Found in faeces and can easily spread to the bladder
Other causes:
-Klebsiella pneumoniae (gram-negative anaerobic rod)
-Enterococcus
-Pseudomonas aeruginosa
-Staphylococcus saprophyticus
-Candida albicans (fungal)
How is a UTI managed
Duration of antibiotics:
-3 days of antibiotics for a simple lower urinary tract infection in women
-5-10 days of antibiotics for women that are immunosuppressed, have abnormal anatomy or impaired kidney function
-7 days of antibiotics for men, pregnant women or catheter related UTIs
NICE recommend changing the catheter when someone is diagnosed with a catheter related urinary tract infection.
Antibiotics Choice:
First line:
-Trimethoprim
-Nitrofurantoin
Alternatives:
-Pivmecillinam
-Amoxicillin
-Cefalexin
How are UTIs treated in pregnancy
Increased risk of pyelonephritis, premature rupture of memranes and pre-term labour
Management:
-7 days of abx (even with asymptomatic bacteruria)
-Urine culture and sensitivities
-First line: nitrofurantoin (1st and 2nd trimester), trimethoprim (2nd and 3rd trimester)
-second line: cefalexin or amoxicillin
Nitrofurantoin is generally avoided in the third trimester as it is linked with haemolytic anaemia in the newborn.
Trimethoprim is generally considered safe in pregnancy but avoided in the first trimester or if they are on another medication that affects folic acid (such as anti-epileptics) due to the anti-folate effects.
How is pyelonephritis managed
Referral to hospital if there are features of sepsis
First line antibiotics for 7-10 days when treating in the community:
-Cefalexin
-Co-amoxiclav
-Trimethoprim
-Ciprofloxacin
What is pyelonephritis
Inflammation of the kidney parenchyma and the renal pelvis typically due to a bacterial infection
What are complicated vs uncomplicated pyelonephritis pictures
Uncomplicated:
-structurally normal urinary tract
-functionally normal urinary tract
-non-immunocompromised host
Complicated:
-Structural or functionally abnormal urinary tract
-Immunocompromised host
-Male (all considered abnormal urinary tract)
What is the pathophysiology of pyelonephritis
Acute pyelonephritis results from bacterial infection of the renal pelvis and parenchyma. Bacteria can reach the kidney either by ascending from the lower urinary tract, directly from the blood stream, as in cases of septicaemia or infective endocarditis or, rarely, via lymphatics (as seen in cases of retroperitoneal abscess).
Neutrophils infiltrate the tubules and interstitium and cause suppurative inflammation. There are often small renal cortical abscesses and streaks of pus in the renal medulla.
The most common organism* (~80%) isolated is Escherichia coli. Other organisms include, Klebsiella, Proteus, Enterococcus faecalis (catheters), Staphylococcus aureus (catheters), Staphylococcus saprophyticus (commensal), and Pseudomonas (catheters).
*Rarely, Mycobacterium spp, yeasts, or other fungi can be the cause in immunocompromised patients
What are the risk factors for pyelonephritis
Factors reducing antegrade flow of urine
-Obstructed urinary tract, including BPH
-Spinal cord injury, resulting in a neuropathic bladder
Factors promoting retrograde ascent of bacteria
-Female gender (due to a short urethra)
-Indwelling catheter or ureteric stents / nephrostomy tubes in-situ
-Structural renal abnormalities, such as vesico-ureteric reflux (VUR)
Factors predisposing to infection or immunocompromise
-Diabetes mellitus
-Corticosteroid use
-HIV infection (untreated)
Factors promoting bacterial colonisation
-Renal calculi
-Sexual intercourse
-Oestrogen depletion (menopause)
What are the differentials for pyelonephritis
Any patient present with back pain and tachycardia and / or hypotension, especially if elderly or with sufficient risk factors, should be assessed for a potential ruptured AAA.
Other differentials:
-renal calculi,
-acute cholecystitis,
-ectopic pregnancy
-pelvic inflammatory disease
-lower lobe pneumonia
-diverticulitis
How is pyelonephritis investigated
Urinalysis:
-nitrites
-leucocytes
-urine beta-HCG (pregnancy)
-urine culture
Routine bloods:
-FBC
-CRP
-U and Es
Renal US looking for evidence of obstruction (infected obstructed system is a urological emergency)
If obstruction is suspected, non-contrast CT imaging of the renal tract should be performed (CT KUB)
What are potential complications of pyelonephritis
Severe sepsis and multiorgan failure, renal scarring leading to chronic kidney disease, pyelonephrosis, and preterm labour in pregnancy
What is chronic pyelonephritis
Repeated infections can lead to chronic pyelonephritis, with such repetitive inflammatory events leading to fibrosis (scarring) and ultimately destruction of the kidney.
More common in obstructed systems resulting in urinary reflux, such as strictures caused by UTIs, VUR, other anatomical abnormalities.
The diagnosis if often made radiologically when evidence of a small, scarred shrunken kidney is seen.
Chronic pyelonephritis is more common in children and can often present asymptomatic or with first presentation as chronic kidney disease.
The mainstay of management is to reverse any underlying causes, optimise renal function, and consider prophylactic antibiotics.
What is emphysematous pyelonephritis
A rare and severe form of acute pyelonephritis, caused by gas-forming bacteria, and is associated with a high-mortality rate.
It presents similar to acute pyelonephritis, however typically will fail to respond to empirical IV antibiotics. CT imaging will show evidence of gas within and around the kidney.
It is most common in diabetic patients, as the high glucose allows CO2 production from fermentation by enterobacteria.
Mild cases can be treated with broad-spectrum anti-microbial cover. Severe cases may warrant either nephrostomy insertion or percutaneous drainage of any collections present; in some cases, nephrectomy may be required
What are the risk factors for UTI
Extremely common in young, sexually active females
Risks:
-recent sexual intercourse
-Diabetes
-History or UTIs
-Spermicide use
-Catheters
What is in the sepsis 6 protocol
3 in:
-O2
-Antibiotics
-IV fluids
3 out:
-Blood cultures
-Urine output
-Lactate
Prompt treatment within 1 hour
How can UTIs be further investigated
Warranted in those who do not respond to treatment, present with severe infection, have an atypical infection or underlying co-morbidities.
FBC and CRp and U and Es
Radiological investigations
-Ultrasound
-CT KUB
-Looking for abscesses, haemorrhage, calculi, obstruction and emphysematous pyelonephritis
What is urinary retention
An inability to pass urine
Can be acute or chronic
Acute urinary retention is define as new onset inability to pass urine which leads to pain and discomfort with significant residual volumes. Modt common in older males, typically due to an enlarged prostate leading to bladder outflow obstruction, however there are a wide array of potential causes.
Chronic urinary retention is the painless inability to pass urine due to long standing retension and so significant bladder distension resulting in bladder desensitisation and therefore minimal discomfort despite poetnial large intra-vesical volumes.
Acute-on-chronic:
Pts with chronic retention can also enter acute retention, either as an acute deterioration of the underlying pathology causing their chronic retention or a new aetiology superimposed on a background of chronic retention.
Will likely have minimal discomfort despite bery large residual volumes.
Should be treated as per acute retention management, however may have much higher residual volumes than other acute retention patients and so more at risk to post-op diuresis.
What is the aetiology of urinary retention
In men, most common cause, is benign prostatic hyperplasia (BPH). Other common obstructive causes include uretrail strictures or prostate cancer
UTIs can cause the urethral sphincter to close, especially in those with already narrowed outflow tracts (eg BPH).
Constipatient can cause acute retention through compression on the urethra
Severe pain can often cause patients to enter acute retention. Medications such as anti-muscarinics or spinal or epidural anaesthesia can affect innervation to the bladder, resulting in acute retention
Neurological causes:
-peripheral neuropathy
-iatrogenic nerve damage during pelvic surgery
-upper motor neurone disease (eg MS or Parkinson’s disease)
-DSD (detrusor sphincter dyssynergia)
What is detrusor sphinter dyssynergia
Lack of coordination of detrusor muscle contraction with urethral sphincter relaxation, leading to contraction against a closed sphincter, often seen with spinal cord pathology or traumatic injury
How does urinary retention present
Acute suprapubic pain
Inability to micturate
Symptoms of the predisposing cause (eg UTI, change of meds)
Palpably distended bladder with suprapubic tenderness
Fevers, rigours or lethargy may suggest infective causes
Must perform a PR exam to look for prostate enlargement or constipation
How is urinary retention investigated
Post void bedside bladder scan will show the volume of retained urine, helping to confirm the diagnosis
All patients require routine bloods, esp FBC, CRP and UandEs
Post catheterisation, a CSU (catheterised specimen of urine) should be sent to assess for the presence of infection.
If a large volume of urine drained on catheterisation (>1L) then high pressure chronic retention (HPCR) should be ruled out (bilateral hydronephrosis or an AKI with no other cause then likely HPCR)
Patients with features of High pressure retention will require an US of their urinary tract to assess for presence of hydronephrosis. If this is confirmed, follow up with repeat imaging in the subsequent weeks following treatment of the retention too ensure its resolution
How is acute urinary retention managed
Immediate urethral catheterisation to resolve the retention. Ensure to measure the volume of drained post-catheterisation
Underlying cuases should be treated accordingly:
-enlarged prostate - appropraiate meds (typically tamsulosin) should be started
-check CSU for infection - treat with abx if appropriate
-review med chart for attribution
TWOC (trial without catheter) attempted once underlying cause is treated and if voids successfully with a minimal residual volume then passes. If fails will be recatheterised. Further TWOCs can be attempted if fails but multiple failed TWOCs may warrant long term catheter, until definitive management arragned to treat underlying cause.
What are the potential complications of acute urinary retention
Few complications if caught and treated early
In those with acute-on-chronic, AKI can occur which can lead to CHD if multiple episodes of retneiton leading to renal scarring
other complcations of increased risk of UTIs and Renal stones due to urinary stasis
WHat is the pathophysiology of chronic urinary retention
Men:
-most common is BPH
-other obstructive causes of urethral strictures or prostate cancer
Women:
-pelvic prolapse (such as cystocele, rectocele or uterine prolapse)
-pelvic masses (such as large fibroids)
Neurological causes:
-peripheral neuropathies
-upper motor neurone disease (Eg MS or Parkinson’s)
How does chronc urinary retention present
Painless urinary retention
Associated voiding LUTS wg weak stream and hesitancy with reduced functional capacity (the ability of the bladder to store urine before producing urge to void)
Overflow incontinence whereby the intra-vesical pressures rise greated than those of the urinary sphincter. Usually worse at night (nocturnal enuresis) when the sphincter tone is reduced
Palpable distended bladder with no or minimal tenderness
Perform PR (in men) to assess for evidence of prostate enlargement
What is high pressure urinary retention
Refers to the urinary retention causing such high intra-vesicular pressures that the anti-reflux mechanism of the bladder and ureters is overcome and ‘backs up’ into the upper renal tract leading to hydroureter and hydronephrosis, impairing the kidneys’ clearance levels.
Such patients present in retention with associated deranged renal function, and hydronephrosis will be subsequently confirmed on imaging (typically ultrasound as first line). Repeat episodes of high-pressure chronic retention can cause permanent renal scarring and chronic kidney disease (CKD).
By contrast, low pressure retention occurs in patients with retention with the upper renal tract unaffected due competent urethral valves or reduced detrusor muscle contractility / complete detrusor failure.
What is post-obstructive diuresis
Following resolution of the retention through catheterisation, the kidneys can often over-diurese due to the loss of their medullary concentration gradient, which can take time to re-equilibrate.
This over-diuresis can lead to a worsening AKI. Consequently, those patients at risk should have their urine output monitored over the following 24 hours post-catheterisation.
Patients producing >200ml/hr urine output should have around 50% of their urine output replaced with intravenous fluids to avoid any worsening AKI.
What are the potential complications of chronic urinary retention
Due to stasis of urine, patients with chronic retention are more likely to develop urinary tract infections and form bladder calculi.
Repeat episodes of unmanaged high-pressure retention can lead to chronic kidney disease.
What is hyperkalaemia
Plasma potassium in excess of ≥ 5.5 mmol/L
Further classified by the European resus guide as:
Mild – 5.5-5.9 mmol/L
Moderate – 6.0-6.4 mmol/L
Severe – >6.5 mmol/L
The incidence of complications rises with increasing severity of hyperkalaemia
The rate at which serum potassium rises also is an important factor which influences the likelihood of complications occurring
What is the aetiology of hyperkalaemia
Renal:
In healthy individuals, the kidneys are responsible for 90% of potassium excretion, with the remainder excreted via the gastrointestinal tract. As a result, renal impairment is one of the commonest causes of hyperkalaemia.
-Acute kidney injury (AKI)
-Chronic kidney disease (CKD)
-Hyperkalaemic renal tubular acidosis
Iatrogenic:
Many medications can cause or contribute to hyperkalemia directly or indirectly:
-ACE inhibitors
-Angiotensin receptor blockers
-Potassium-sparing diuretics
-NSAIDs/COX 2 inhibitors
-Digoxin (in toxicity)
-Trimethoprim
-Beta-blockers – selective and non-selective can cause it
-Nicorandil
-Heparin – unfractionated and LMWH
-Ciclosporin
-Tacrolimus
-Renin-inhibitors (e.g. aliskiren)
-Potassium supplements
Intravenous fluids containing potassium also have the potential to cause hyperkalaemia when prescribed inappropriately.
Blood transfusion is another potential cause of hyperkalaemia.
Trauma and burns:
Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells.
DKA:
In diabetic ketoacidosis (DKA) potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalaemia.
Addison’s:
Aldosterone promotes excretion of potassium by the kidneys.
In Addison’s disease, the adrenal glands are unable to produce adequate levels of aldosterone which results in reduced renal excretion of potassium.
What results in a pseudohyperkalaemia picture
Pseudohyperkalaemia can occur for a wide variety of reasons including:
-Haemolysis (e.g. prolonged tourniquet time, prolonged sample transport time, use of incorrect blood bottles)
-Blood sample being taken from a limb receiving IV fluids containing potassium
-Leukocytosis and thrombocytosis
If there are concerns about pseudohyperkalaemia, a sample should be urgently repeated to check the validity of the result.
How does hyperkalaemia present
Typically vague symptoms of general weakness and fatigue
May sometimes experience:
-palpitations
-chest pain
-SOB
No obvious signs of hyperkalaemia usually
Potentially:
-bradicardia secondary to hyperkalaemia0induced atrioventricular block
-depressed or absent tendon reflexes
How is hyperkalaemia investigated
U&Es should be performed to:
-confirm the presence of hyperkalaemia and assess other electrolytes (a repeat sample should be sent if hyperkalaemia is noted)
-assess renal function (the kidneys are responsible for 90% of potassium excretion)
FBC should be performed to:
-rule out haemolysis (e.g. normocytic normochromic anaemia)
-rule out leukocytosis or thrombocytosis
Capillary blood glucose should be performed to rule out hyperglycaemia (e.g. DKA).
An arterial blood gas should be performed to rule out metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA).
Serum cortisol should be performed to rule out Addison’s disease (low serum cortisol is found in Addison’s).
A digoxin level should be performed to rule out toxicity (if relevant).
An ECG is an essential investigation in the context of hyperkalaemia, abnormalities can include:
-Tall tented T waves
-Wide QRS complexes
-Prolonged PR interval
-Flattened P waves
-AV block
-Bradycardia
How is hyperkalaemia managed
The urgency by which hyperkalemia needs to be treated is determined by the level of potassium and the presence/absence of associated ECG changes.
A potassium level of ≥7.0 mmol/L and/or a patient with hyperkalaemia associated ECG changes requires URGENT treatment.
All patients with hyperkalaemia will ultimately require some form of further monitoring and management.
Step 1.Prevent further accumulation of potassium:
-Stop any intravenous fluids containing potassium
-Suspend any medications that have the potential to increase serum potassium
-Suspend any supplements containing potassium
Step 2.Stabilise the cardiac membrane:
-Administer intravenous calcium gluconate (10mls of 10% solution) if there are hyperkalaemia associated ECG changes present. This should help to stabilise the myocardium temporarily for 30-60 minutes and reduce the risk of fatal arrhythmia.
-Further doses may be required if ECG changes persist (you would expect ECG changes to begin to improve within 1-3 minutes from the administration of calcium gluconate). The administration of calcium gluconate in the absence of hyperkalaemia associated ECG changes is not recommended.
Step 3.Shift potassium intracellularly:
-Insulin-glucose infusion: insulin helps to shift potassium from the extracellular to the intracellular compartment, whilst the glucose helps to maintain capillary blood glucose levels.
-Salbutamol: often used as adjuvant therapy for hyperkalaemia as it promotes the movement of potassium into cells and therefore out of the serum.
Step 4.Remove potassium from the body:
-Calcium polystyrene sulfonate resin (Calcium resonium) can be used to remove potassium via the gastrointestinal tract.
-Correction of the underlying cause: the kidneys should then be able to resume their normal function of excreting adequate volumes of potassium via the urine.
-Haemodialysis is an invasive treatment reserved as a last resort for resistant hyperkalaemia that has failed to respond to all other therapies.
