Critical care: neuro and renal Flashcards
Describe mechanism of TURP syndrome
-Irrigation fluid for TURP is hypo-osmolar
-Hyposmolar solution used to avoid diathermy injury to pt from resectoscope
-If absorbed via prostatic venous sinuses: can result in hyponatraemia and hypervolaemia
Why does TURP syndrome cause change in bp?
- Volume overload initially causes hypertension
- Subsequently causes cardiac insufficiency and hypotension
What is TURP syndrome?
-Caused by absorbtion of large amounts of irrigation fluid into prostatic venous sinuses
-Syndrome can be caused by hyponatraemia (<125mmol/L) or hyperammonaemia (metabolite of glycine)
What are signs and symptoms of TURP syndrome?
-Hypertension and then hypotension
-Tachycardia
-Hypoxia (overload)
-Dyspnoea (overload)
-neurological: confusion, disorientation, convulsions, coma
What is the mechanism behind neurological symptoms in TURP syndrome?
Hyponatreamia causes osmotic gradient in the brain resulting in cerebral oedema and raised ICP
What are the most appropriate irrigation fluids for use in TURP syndrome?
Hypoosmar solutes (Glycine, Sorbitol, Manitol)
How would you manage hypotensive patient with TURP syndrome?
Resuscitate according to Ccrisp protocol
Identify bleeding, take bloods including osmolality
Stop IVI
Inform ITU/HDU and operating surgeon
Where should hypotensive pt with TURP syndrome be managed?
in ITU/HDU
Risk of developing cerebral/pulmonary oedema
What precautions can be taken to minimise risk of TURP?
Minimise operating time
Close monitoring of observations during surgery
Keep fluid bag low to reduce pressure
Minimise operative bleeding
How is hyponatraemia classified?
Hypervolaemic: Excess water dilutes sodium
Euvolaemic: Hyponatraemia in presence of normal water levels
Hypovolaemic: water and sodium levels are both low
What are causes of hypervolaemic hyponatraemia?
Renal failure, liver failure, heart faliure, iatrogenic fluid overload
What are causes of euvolaemic hyponatraemia?
SIADH
Hypothyroidism
What are causes of SIADH?
-CNS causes: mass/bleed (trauma, sah), infection (meningitis)
-Pulmonary causes (pneumonia, asthma
-Cancer: gi, lung, genitourinary
-Drugs: (SSRI)
What are causes of hypovolaemic hyponatraemia?
-Marked blood loss
-Inadequate replacement of fluid and electrolytes
-sepsis
How is sodium reabsorbed by the kidneys?
Majory (60%) of filtered sodium is reabsorbed in the PCT via an ATP dependent pump
-20% loop of henle: passive due to countercurrent mechanism
-remainder dct and collecting ducts under control of aldosterone (active)
What is absorbed in proximal convoluted tubule?
Sodium reabsorption (60%) via ATP dependent pump
Passive reabsorption of chloride ions
Water reabsorption down osmotic gradient
What is absorbed in loop of henle?
Loop of henle reabsorbs 25% filtered sodium
Passive reabsorption of chloride ions
Ascending limb impermeable to water
Reabsorption of water in descending limb down osmotic gradient
What is absorbed in loop of henle?
Sodium reabsorption (25%)
Passive reabsorption of chloride ions
Ascending limb impermeable to water
Loop of henle reabsorbs 25% of filtered sodium
What is absorbed in distal convoluted tubule?
-Sodium reabsorption (8%). This process is energy dependent.
-Reabsorption of sodium in dct and collecting duct is partially under control of aldosterone
-Low osmolality of ultrafiltrate entering dct leads to passive reabsorption of water, which continues in collecting ducts
Explain the countercurrent mechanism
-formed by two parallel limbs in loop of henle
-Ascending limb is highly impermeable to water but permeable to solutes (Na, Cl)
-Reabsorption of solutes creates osmotic gradient in medullary interstitium and raises osmolality of this compartment
-Leads to reabsorption of water from descending limb
Define acute renal failure
Sudden impairment of the kidney’s ability to excrete nigtrogenous waste products of metabolism
Causes of pre-renal failure
Dehydration
Sepsis
Heart failure
Blood loss
Causes renal AKI
-ATN
-Glomerulonephritis
-Hepatorenal syndrome
-Vasculitis
-Nephrotoxic medications
Causes Post renal AKI
Obstruction from calculi
Prostatic obstruction (BPH, Cancer)
Renal/bladder tumour
Extrinsic compression from pelvic tumours
What is the pathogenesis of acute renal failure?
-reduced perfusion pressure -> efferent vasoconstriction -> reduced blood flow and cortical/medullary ischaemia -> shedding cells into lumen -> back leak fluid into insterstitium -> increased medullary hydrostatic pressure—> reduced re absorption
renal parenchyma ischaemia results from fall in perfusion pressure
-This leads to vasoconstriction of efferent arterioles which preserves capillary filtration pressure
-Contricted efferent arterioles have reduced blood flow, resulting in worsening cortical and medullary ischaemia
-Ischaemic cells are shed into tubular lumen causing obstruction, which promotes a ‘back leak’ of tubular fluid into interstitium
-This raises interstitial hydrostatic pressure, which reduces tubular fluid reabsorption and worsens oliguria
Which part of nephron will be affected by acute renal failure first?
-thick ascending limb—> within medulla, most atp pumps
Cells of thick ascending limb are most susceptible to ischaemic injury
-This is because they are within medulla, which has poorer oxygenation than cortex
-Also, active ATP pumps at cell membrane have higher oxygen demand
Where is renin released from in kidneys and what triggers its release?
-Renin is released from juxtaglomerular apparatus
Renin release is triggered by:
-Reduced renal perfusion
-Sympathetic nervous system stimulation
-Catecholamine release
-Hyponatraemia
Renin cleaves angiotensin 1 from angiotensinogen
Name some nephrotoxic drugs
NSAIDS
ACE inhibitors
Gentamicin
Furosemide
Thiazide diuretics
Name some important life-threatening complications of acute renal failure
-Fluid retention and hypervolaemia leading to acute pulmonary oedema
-Hyperkalaemia leading to metabolic acidosis and cardiac arrythmias
How would you manage hypperkalaemia?
10ml 10% calcium gluconate
Insulin dextrose infusion
Salbutamol
Calcium resonium
Treat cause
What are the indications for renal replacement therapy?
Acidosis
Refractory hyperkalaemia
Refractory pulmonary oedema and fluid overload
Uraemic encephalopathy
Removal of toxins
Grade 1 kidney injury
Renal contusion, non-expanding subcapsular haematoma
Grade 2 kidney injury
Laceration <1cm in depth not involving renal medulla and collecting system, non-expanding retroperitoneal haematoma
grade 3 kidney injury
Laceration >1cm not involving collecting system
grade 4 kidney injury
Laceration >1cm extending into collecting system, renal vessel injury with haemorrhage
Grade 5 kidney injury
Shattered kidney or avulsed renal vessels
What are the indications for surgical management of renal trauma?
Haemodynamically unstable patient indicating ongoing bleeding
Expanding perinephric haematoma
Avulsion of renal pedical
When would you suspect urethral injury in a patient?
-Bleeding from urethra
-Perineal haematoma
-Scrotal haematoma
-High riding prostate on DRE in male
What is the likely anatomical site of urethral injury in a male in pelvic ring fractures and in ‘saddle injuries’?
Pelvic ring fractures: membranous part of urethra
-Saddle injuries: bulbar urethra
What investigation would you do to confirm urethral injuries?
Retrograde urethrogram
How woulld you manage a patient with suspected urethral injury?
If there is no extravasation on retrograde urethrogram, urinary catheter
If there is extravasation, suprapubic
Formal surgical repair can be considered at later stage.
GCS: Eyes
4: Eyes open spontaneously
3: Eye open to verbal command
2: Eye open to pain
1: No eye response
GCS: Best verbal response:
5: Orientated
4: Confused
3: Inappropriate words
2: Incomprehensible sounds
1: No verbal response
Best motor response
6: Obeys commands
5: Localises to pain
4: Withdraws from pain
3: Flexion to pain
2: Extension to pain
1: No motor response
Indications for CT head within 1 hr:
-GCS <13 on initial assessment in emergency -department
-GCS <15 at 2 hrs after the injury on assessment in emergency department
-Suspected open or depressed skull fracture
-Any sign basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign
-Post traumatic seizure
-Focal neurological deficit
-> 1 episode vomiting
Indications for CT head within 8 hrs
In those who have had some LOC or amnesia:
-Age 65 or older
-Any history of bleeding or clotting disorders
-Dangerous mechnism (Fall >1m, 5 stairs, pedestrian or cyclist struck by vehicle, occupant ejected from vehicle)
->30mins amnesia of events immediately before injury
-anticoagulation
What are different categories for CT head indications in nice guidelines?
CT within 1 hr
CT within 8 hrs
What is cushing’s reflex?
-Mixed vagal and sympathetic stimulation that occurs in response to raised ICP
-Results in hypertension and bradycardia
Cushings triad:
-irregular decreased respirations (due to decreased brain stem function)
-systolic hypertension (widened pulse pressure)
-bradycardia
How is cerebral perfusion pressure calculated?
Mean arterial pressure - intracranial pressure
In what circumstances would it be appropriate to admit a pt with a head injury?
-When CT not available
-Abnormal CT
-Prolonged loss of or deteriorating consciousness/abnormal GCS
-Focal neurological deficit
-Headache
-Penetrating head injury/skull fracture
-Alcohol/drug intoxication
-CSF leak (rhinorrhea/otorrhea)
What is definition of brainstem death?
Defined as irreversible cessation of brainstem function
What preconditions need to be met for a diagnosis of brainstem death?
-Apnoeic coma requiring ventilation and a known cause of irreversible brain damage
-Pt not sedated
Brainstem death test: Pupil responses (nerves involved and reaction)
-CN II, III
-No direct/indirect reaction to light
Brainstem death test: Corneal reflex
-CN V,VII
-No reaction to direct stimulation with cotton wool
Brainstem death test: Pain reflex
-CN V and VII
-Pain tested in facial distribution
-Brainstem death cannot be diagnosed if response to central pain
Brainstem death test: Caloric test
-CN 3, 6, 8
-Cold water instilled into auditory canal, nystagmus towards stimulation is looked for
-Absent in brainstem death
Brainstem death test: Gag reflex
-CN 9 and 10
Brainstem death test: apnoea test
-Pre-oxygenate and then disconnect from ventilator
-Insufflate oxygen into trachea, observe for sign of respiration until PaCO2 is above 6.65 kPa
What are creterion for performance of brainstem death tests?
-2 doctors on 2 separate occasions
-Each must be >5 years post full GMC registration
-Death is deemed to have occured after first set of tests, this is time on death cert.
What tests of brainsteam death are there?
-Pupil responses
-Corneal reflex
-pain reflex
-Caloric test
-Gag reflex
-Apnoea test
-If there are no signs to these tests when performed by appropriate clinicians, brainstem death can be diagnosed
What are symptoms of raised ICP?
-Headache
-Nausea and vomiting
-Reduced level of consciousness
What is normal ICP?
0-10mmhg in adults in supine position
Explain Monro-Kellie doctrine
-Cranial vault is fixed space consisting of 3 components: blood (10%), CSF (10%), Brain parenchyma (80%)
-Expansion of any one of these components results in compensatory decrease to maintain ICP
-When compensatory mechanism is exhausted, there is an exponential increase in ICP even with small increase in volume of increased content/mass
What are effects of raised ICP
-Decreased cerebral perfusion pressure causing iscahemia
-Midline shift causing ventricular obstruction
-Brain herniation, coma, eventually death
How can ICP be reduced?
Reduced blood
-Regulate ventilation to maintain PaCO2 4-4.5 kPa (infreased vasoconstriction)–> co2 is vasodilator
-Use of hypertonic saline
-Diuretics: mannitol 20% 0.25-0.5 g/kg
-Upward tilt of head of bed to 20 degrees
Reduced CSF
-Direct tapping CSF from ventricular catheter
Reduced parenchyma
-Surgical debulking
-Craniectomy
Other
-Steroids may reduce swelling around tumours, but not in trauma situation
-Barbiturate coma
-Sedation +/- use of paralysis (reduced mro2)
How can ICP be monitored?
-Subarachnoid bolt
-Epidural bolt (less accurate, less infection risk)
-External ventricular drain (can use to therapeutically remove csf)
What investigations would you perform for renal acolic?
Bloods: U + E, Bone profile, urate
Imaging: CTKUB, US if pregnant
What are the common sites of stone impaction along the ureter?
-Pelvi-ureteric junction
-When the ureter crosses pelvic brim
-Vesico-ureteric junction
What are the different types of renal stones?
Calcium oxalate stones
Calcium phosphate stones
Struvite stone: magnesium and ammonia (also known as infection stone)
Uric acid stone
What is a staghorn calculus?
Stone occupying renal pelvis and at least one calyceal system
Which stones can you manage conservatively?
Stones <4mm will almost always pass spontaenoiusly
How would you manage pt with a stone >1cm and impaired renal function?
-Ureteric stent placement
-Percutaneous nephrostomy
How would you manage renal stones?
-Conservative management
-Ureteroscopy and stone retrieval
-ESWL
-Percutaneous nephrolithotomy
What are the causes of haematuria?
Infection:
-Cystitis
-Prostatitis
Autoimmune
-Glomerulonephritis
-Iga nephropathy
Tumours
Renal stones
Trauma
What investigations would you consider in pt with haematuria?
-Bloods
-Renal US
-Flexible cystoscopy
-CT urogram
What are the different types of renal tumours?
Benign
-Adenoma
-Angiomyolipoma
-Cysts
Malignant
-Wilm’s tumour
-RCC
-TCC
