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MRCS Critical care > Critical care: neuro and renal > Flashcards

Critical care: neuro and renal Flashcards

1
Q

Describe mechanism of TURP syndrome

A

-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

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2
Q

Why does TURP syndrome cause change in bp?

A
  1. Volume overload initially causes hypertension
  2. Subsequently causes cardiac insufficiency and hypotension
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3
Q

What is TURP syndrome?

A

-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)

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4
Q

What are signs and symptoms of TURP syndrome?

A

-Hypertension and then hypotension
-Tachycardia
-Hypoxia (overload)
-Dyspnoea (overload)
-neurological: confusion, disorientation, convulsions, coma

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5
Q

What is the mechanism behind neurological symptoms in TURP syndrome?

A

Hyponatreamia causes osmotic gradient in the brain resulting in cerebral oedema and raised ICP

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6
Q

What are the most appropriate irrigation fluids for use in TURP syndrome?

A

Hypoosmar solutes (Glycine, Sorbitol, Manitol)

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7
Q

How would you manage hypotensive patient with TURP syndrome?

A

Resuscitate according to Ccrisp protocol
Identify bleeding, take bloods including osmolality
Stop IVI
Inform ITU/HDU and operating surgeon

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8
Q

Where should hypotensive pt with TURP syndrome be managed?

A

in ITU/HDU
Risk of developing cerebral/pulmonary oedema

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9
Q

What precautions can be taken to minimise risk of TURP?

A

Minimise operating time
Close monitoring of observations during surgery
Keep fluid bag low to reduce pressure
Minimise operative bleeding

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10
Q

How is hyponatraemia classified?

A

Hypervolaemic: Excess water dilutes sodium
Euvolaemic: Hyponatraemia in presence of normal water levels
Hypovolaemic: water and sodium levels are both low

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11
Q

What are causes of hypervolaemic hyponatraemia?

A

Renal failure, liver failure, heart faliure, iatrogenic fluid overload

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12
Q

What are causes of euvolaemic hyponatraemia?

A

SIADH
Hypothyroidism

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13
Q

What are causes of SIADH?

A

-CNS causes: mass/bleed (trauma, sah), infection (meningitis)
-Pulmonary causes (pneumonia, asthma
-Cancer: gi, lung, genitourinary
-Drugs: (SSRI)

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14
Q

What are causes of hypovolaemic hyponatraemia?

A

-Marked blood loss
-Inadequate replacement of fluid and electrolytes
-sepsis

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15
Q

How is sodium reabsorbed by the kidneys?

A

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)

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16
Q

What is absorbed in proximal convoluted tubule?

A

Sodium reabsorption (60%) via ATP dependent pump
Passive reabsorption of chloride ions
Water reabsorption down osmotic gradient

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17
Q

What is absorbed in loop of henle?

A

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

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18
Q

What is absorbed in loop of henle?

A

Sodium reabsorption (25%)
Passive reabsorption of chloride ions
Ascending limb impermeable to water
Loop of henle reabsorbs 25% of filtered sodium

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19
Q

What is absorbed in distal convoluted tubule?

A

-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

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20
Q

Explain the countercurrent mechanism

A

-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

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21
Q

Define acute renal failure

A

Sudden impairment of the kidney’s ability to excrete nigtrogenous waste products of metabolism

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22
Q

Causes of pre-renal failure

A

Dehydration
Sepsis
Heart failure
Blood loss

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23
Q

Causes renal AKI

A

-ATN
-Glomerulonephritis
-Hepatorenal syndrome
-Vasculitis
-Nephrotoxic medications

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24
Q

Causes Post renal AKI

A

Obstruction from calculi
Prostatic obstruction (BPH, Cancer)
Renal/bladder tumour
Extrinsic compression from pelvic tumours

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25
Q

What is the pathogenesis of acute renal failure?

A

-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

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26
Q

Which part of nephron will be affected by acute renal failure first?

A

-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

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27
Q

Where is renin released from in kidneys and what triggers its release?

A

-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

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28
Q

Name some nephrotoxic drugs

A

NSAIDS
ACE inhibitors
Gentamicin
Furosemide
Thiazide diuretics

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29
Q

Name some important life-threatening complications of acute renal failure

A

-Fluid retention and hypervolaemia leading to acute pulmonary oedema
-Hyperkalaemia leading to metabolic acidosis and cardiac arrythmias

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30
Q

How would you manage hypperkalaemia?

A

10ml 10% calcium gluconate
Insulin dextrose infusion
Salbutamol
Calcium resonium
Treat cause

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31
Q

What are the indications for renal replacement therapy?

A

Acidosis
Refractory hyperkalaemia
Refractory pulmonary oedema and fluid overload
Uraemic encephalopathy
Removal of toxins

32
Q

Grade 1 kidney injury

A

Renal contusion, non-expanding subcapsular haematoma

33
Q

Grade 2 kidney injury

A

Laceration <1cm in depth not involving renal medulla and collecting system, non-expanding retroperitoneal haematoma

34
Q

grade 3 kidney injury

A

Laceration >1cm not involving collecting system

35
Q

grade 4 kidney injury

A

Laceration >1cm extending into collecting system, renal vessel injury with haemorrhage

36
Q

Grade 5 kidney injury

A

Shattered kidney or avulsed renal vessels

37
Q

What are the indications for surgical management of renal trauma?

A

Haemodynamically unstable patient indicating ongoing bleeding
Expanding perinephric haematoma
Avulsion of renal pedical

38
Q

When would you suspect urethral injury in a patient?

A

-Bleeding from urethra
-Perineal haematoma
-Scrotal haematoma
-High riding prostate on DRE in male

39
Q

What is the likely anatomical site of urethral injury in a male in pelvic ring fractures and in ‘saddle injuries’?

A

Pelvic ring fractures: membranous part of urethra
-Saddle injuries: bulbar urethra

40
Q

What investigation would you do to confirm urethral injuries?

A

Retrograde urethrogram

41
Q

How woulld you manage a patient with suspected urethral injury?

A

If there is no extravasation on retrograde urethrogram, urinary catheter

If there is extravasation, suprapubic

Formal surgical repair can be considered at later stage.

42
Q

GCS: Eyes

A

4: Eyes open spontaneously
3: Eye open to verbal command
2: Eye open to pain
1: No eye response

43
Q

GCS: Best verbal response:

A

5: Orientated
4: Confused
3: Inappropriate words
2: Incomprehensible sounds
1: No verbal response

44
Q

Best motor response

A

6: Obeys commands
5: Localises to pain
4: Withdraws from pain
3: Flexion to pain
2: Extension to pain
1: No motor response

45
Q

Indications for CT head within 1 hr:

A

-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

46
Q

Indications for CT head within 8 hrs

A

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

47
Q

What are different categories for CT head indications in nice guidelines?

A

CT within 1 hr
CT within 8 hrs

48
Q

What is cushing’s reflex?

A

-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

49
Q

How is cerebral perfusion pressure calculated?

A

Mean arterial pressure - intracranial pressure

50
Q

In what circumstances would it be appropriate to admit a pt with a head injury?

A

-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)

51
Q

What is definition of brainstem death?

A

Defined as irreversible cessation of brainstem function

52
Q

What preconditions need to be met for a diagnosis of brainstem death?

A

-Apnoeic coma requiring ventilation and a known cause of irreversible brain damage
-Pt not sedated

53
Q

Brainstem death test: Pupil responses (nerves involved and reaction)

A

-CN II, III
-No direct/indirect reaction to light

54
Q

Brainstem death test: Corneal reflex

A

-CN V,VII
-No reaction to direct stimulation with cotton wool

55
Q

Brainstem death test: Pain reflex

A

-CN V and VII
-Pain tested in facial distribution
-Brainstem death cannot be diagnosed if response to central pain

56
Q

Brainstem death test: Caloric test

A

-CN 3, 6, 8
-Cold water instilled into auditory canal, nystagmus towards stimulation is looked for
-Absent in brainstem death

57
Q

Brainstem death test: Gag reflex

A

-CN 9 and 10

58
Q

Brainstem death test: apnoea test

A

-Pre-oxygenate and then disconnect from ventilator
-Insufflate oxygen into trachea, observe for sign of respiration until PaCO2 is above 6.65 kPa

59
Q

What are creterion for performance of brainstem death tests?

A

-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.

60
Q

What tests of brainsteam death are there?

A

-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

61
Q

What are symptoms of raised ICP?

A

-Headache
-Nausea and vomiting
-Reduced level of consciousness

62
Q

What is normal ICP?

A

0-10mmhg in adults in supine position

63
Q

Explain Monro-Kellie doctrine

A

-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

64
Q

What are effects of raised ICP

A

-Decreased cerebral perfusion pressure causing iscahemia
-Midline shift causing ventricular obstruction
-Brain herniation, coma, eventually death

65
Q

How can ICP be reduced?

A

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)

66
Q

How can ICP be monitored?

A

-Subarachnoid bolt
-Epidural bolt (less accurate, less infection risk)
-External ventricular drain (can use to therapeutically remove csf)

67
Q

What investigations would you perform for renal acolic?

A

Bloods: U + E, Bone profile, urate
Imaging: CTKUB, US if pregnant

68
Q

What are the common sites of stone impaction along the ureter?

A

-Pelvi-ureteric junction
-When the ureter crosses pelvic brim
-Vesico-ureteric junction

69
Q

What are the different types of renal stones?

A

Calcium oxalate stones
Calcium phosphate stones
Struvite stone: magnesium and ammonia (also known as infection stone)
Uric acid stone

70
Q

What is a staghorn calculus?

A

Stone occupying renal pelvis and at least one calyceal system

71
Q

Which stones can you manage conservatively?

A

Stones <4mm will almost always pass spontaenoiusly

72
Q

How would you manage pt with a stone >1cm and impaired renal function?

A

-Ureteric stent placement
-Percutaneous nephrostomy

73
Q

How would you manage renal stones?

A

-Conservative management
-Ureteroscopy and stone retrieval
-ESWL
-Percutaneous nephrolithotomy

74
Q

What are the causes of haematuria?

A

Infection:
-Cystitis
-Prostatitis

Autoimmune
-Glomerulonephritis
-Iga nephropathy

Tumours
Renal stones
Trauma

75
Q

What investigations would you consider in pt with haematuria?

A

-Bloods
-Renal US
-Flexible cystoscopy
-CT urogram

76
Q

What are the different types of renal tumours?

A

Benign
-Adenoma
-Angiomyolipoma
-Cysts

Malignant
-Wilm’s tumour
-RCC
-TCC

MRCS Critical care (11 decks)

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