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Semester 1 ( 3rd Year) > Case 8: An acutely unwell patient > Flashcards

Case 8: An acutely unwell patient Flashcards

1
Q

what is flank pain?

A

on the side of the back below the ribs and above the hips

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2
Q

what could flank pain indicate?

A

kidney stones
infection
muscle strains

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3
Q

what pathologies are relevant to the right hypochondrium abdominal quadrant?

A

acute hepatitis
biliary colic
cholangitis
cholecystitis
pneumonia (referred pain)

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4
Q

what pathologies are relevant to left hypochondrium abdominal quadrant

A

splenomegaly
splenic abscess
splenic infarction
splenic rupture
pneumonia (referred pain)

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5
Q

which pathologies are relevant to epigastrium abdominal quadrant

A

acute myocardial infarction
acute/chronic pancreatitis
gastroesophageal reflux disease
peptic ulcer

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6
Q

which pathologies are relevant to right iliac fossa abdominal quadrant

A

appendicitis
hernias
renal calculi

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7
Q

which pathologies are relevant to left iliac fossa abdominal quadrant

A

diverticulitis
hernias
renal calculi

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8
Q

which pathologies are relevant to hypogastrium (suprapubic) abdominal region

A

bladder retention
cystitis

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9
Q

what symptoms suggest upper urinary tract infection

A

acute colicky abdominal pain
dysuria
fever
vomting

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10
Q

what symptoms suggest diverticulitis/gastroenteritis

A

new diarrhoea and vomiting
abdominal pain
fever

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11
Q

which tool can screen for frailty

A

rockwood frailty score
scored 1-9
1= very fit
9= terminally ill

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12
Q

why would you do a venous blood gas

A

for information on acid-base balance and lactate level

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13
Q

what findings suggest sepsis

A

hypotension
tachycardia
pyrexia
mottled skin
reduced conscious level

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14
Q

what is the sepsis 6

A

take 3- venous blood gas (for lactate), urine output, blood culture

give 3- antibiotics, IV fluids, oxygen

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15
Q

what is definition of sepsis

A

life-threatening organ dysfunction caused by dysregulated host response to infection
it happens when the infection becomes so severe the hosts response to infection goes from being helpful to unhelpful

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16
Q

what is the end result of sepsis

A

tissue hypoxia
mitochondrial dysfunction
macrovascular and microvascular dysfunction
apoptosis

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17
Q

what is definition of septic shock

A

subset of sepsis which describes circulatory, cellular and metabolic abnormalities which are associated with a greater risk of mortality than sepsis alone

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18
Q

when would you suspect septic shock in hospital patients

A

when patients fail to respond to initial treatment
sepsis with persistent hypotension despite fluid correction and iontropes and a serum lactate of greater than 2mmol/L

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19
Q

source of sepsis in CNS

A

meningitis
encephalitis
cerebral/epidural abscesses
discitis

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20
Q

respiratory sources of sepsis

A

pneumonia
lung abscess

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21
Q

cardiac sources of sepsis

A

endocarditis
myocarditis

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22
Q

skin/soft tissue sources of sepsis

A

cellulitis
infected bites/ulcers/wounds
necrotising fasciitis

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23
Q

genitourinary sources of sepsis

A

pyelonephritis
cystitis
obstructed renal calculus

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24
Q

GI sources of sepsis

A

gall bladder infections (cholecystitis, cholangitis)
diverticulitis
infective colitis
appendicitis
tonsilitis

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25
Q

orthopaedic sources of sepsis

A

septic arthritis
prosthetic joint infections

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26
Q

infected lines/devices sources of sepsis

A

peritoneal catheters
tunnel lines
central venous catheters

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27
Q

what fluid is given for sepsis

A

fluid resuscitation is with a crystalloid given as a bolus over less then 15 minutes
500mL of 0.9% Hartmanns solution

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28
Q

what are crystalloids

A

solutions containing small molecules of water

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29
Q

examples of crystalloids

A

sodium chloride
glucose
Hartmanns

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30
Q

what are colloids

A

solutions with large molecular weight molecules

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31
Q

examples of colloids

A

albumins
gelatins

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32
Q

why is lactate raised in sepsis

A

tissue hypoxia as a result of widespread systemic inflammation
there is organ hypo perfusion and subsequently cells turn to anaerobic metabolism which produces lactate

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33
Q

what might hyperkalaemia look like on ECG

A

tall tented T waves
broad QRS complexes (>0.12ms)
no discernible P waves

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34
Q

causes of hyperkalaemia

A

reduced renal excretion of K+

increasing circulating serum potassium- can be exogenous (from K+ supplementation) or endogenous (tumour lysis syndrome, rhabdomyolysis, burns)

pseudohyperkalaemia- there isnt a true election in serum K+ (suspect this in people who have had repeat blood tests done)

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35
Q

when would you need to urgently treat hyperkalaemia

A

when serum K+ exceeds 6.5 and/or there are ECG changes

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36
Q

what are the priorities when treating hyperkalaemia

A

protecting cardiac membrane- IV calcium gluconate

shifting K+ intracellularly- 10 units of insulin with 25g of glucose , actrapid + dextrose

stopping any contributing medications- ACE inhibitors, potassium sparing diuretics

37
Q

what should you do following administering each fluid in sepsis

A

repeat BP

38
Q

what are the kidneys 3 main functions

A

filter and excrete nitrogenous waste products

maintain acid-base balance by controlling reabsorption and excretion of electrolytes (Na, K, Cl)

produce certain hormones (erythemaropoietin, renin, calcitrol)

39
Q

what is a good marker for eGFR of kidneys

A

creatinine (waste product) as it is completely filtered in the glomerulus

40
Q

what is the role of RAAS

A

increase blood pressure
it acts to increase the overall effective circulating volume by:
increasing reabsorption of Na+
and
vasoconstricting efferent arterioles

41
Q

what causes acute tubular necrosis

A

usually the result of a combination of factors which have caused renal ischaemia and toxicity, for example hypotension and dehydration or sepsis with associated nephrotoxic drugs

42
Q

does acute tubular necrosis have high mortality

A

yes at around 50% but it is usually to do with the associated illness such as septic shock

43
Q

complications of AKI

A

the loss of the homeostatic functions of the kidney means the kidneys are:

unable to regulate acid-base balance leading to hyperkalaemia, fluid retention and metabolic acidosis

unable to excrete metabolic waste products leading to a build up of urea and creatinine

this eventually leads to multi organ failure

44
Q

what can the end effects of AKI be on other parts of body

A

encephalopathy- uremic toxins and inflammatory mediators

heart failure- fluid overload, arrhythmia owing to hyperkalaemia

intestinal and microbiota distributions- fluid congestion, ischaemia, acidosis, changes in microbiota secretome, barrier translocations

bone marrow and immune system effects- cytopenia, systemic inflammation, acquired immunodeficiency

liver dysfunction- fluid overload, systemic inflammation

lung injury- fluid overload, kidney cell debris-related microvascular injury

45
Q

why is clotting measured in sepsis patients

A

sepsis can be a cause of disseminated intravascular coagulation (DIC)

46
Q

causes of disseminated intravascular coagulation (DIC)

A

sepsis
trauma
malignancy
obstetric complications (amniotic fluid embolism, placental abruption)

47
Q

why does disseminated intravascular coagulation (DIC) happen

A

tissue factor is released into bloodstream as a result of cytokine release, endotoxin release or endothelial damage

this activates the coagulation pathway

widespread coagulation consumes clotting factors which causes bleeding in addition to macrovascular thrombosis

48
Q

management of disseminated intravascular coagulation (DIC)

A

treat underlying cause

supportive blood product (platelet or FFP) transfusions in life-threatening bleeding, severe thrombocytopenia or when patients need to undergo urgent invasive interventions without delay

49
Q

what is the definition of AKI

A

clinical syndrome characterised by an acute reduction in renal function leading to a rise in serum creatinine and/or decline in urine output

50
Q

3 categorises of AKI causes

A

pre-renal- reduced perfusion of the kidneys either from hypovolemia, reduced renal BF or reduced CO which leads to reduced GFR

renal (intrinsic)- structural damage to the glomeruli, interstitium and/or tubules

post-renal- acute obstruction of urinary flow which increases intra-tubular pressures and subsequently decreases GFR

51
Q

what is the most common cause of AKI

A

pre-renal= 85%
renal= 10%
post-renal= 5%

52
Q

pre-renal causes of AKI

A

dehydration
sepsis
hypotension
shock
hepatorenal syndrome
severe heart failure
hypertension/compartment syndrome

53
Q

renal causes of AKI

A

NSAIDs
ACEi
ARBs
gentamicin
GN/vasculitis
contrast
interstitial nephritis
myeloma
rhabdomyolysis

54
Q

post-renal causes of AKI

A

prostatic enlargement
renal stones
pelvic cancer

55
Q

risk factors for AKI

A

over 65

history of AKI

symptom/history of urological obstruction

chronic conditions- heart failure, liver disease, diabetes

neurological/cognitive impairment or disability (which may limit fluid intake due to reliance on carer)

sepsis

hypovolaemia

oliguria

nephrotoxic drug use within last week

exposure to iodinated contrast agents within the past week

56
Q

history of pre-renal AKI

A

poor oral intake/dehydration
diarrhoea or vomiting

57
Q

history of renal AKI

A

fever, rash, joint pain, nasal crusting, weight loss

long lie history

NSAIDs use

nephrotoxic drug use

58
Q

history of post-renal AKI

A

lower UTI symptoms in men

history of renal calculi (may cause hydronephrosis and obstruction)

59
Q

examination of pre-renal AKI

A

signs of sepsis

slow cap refil, low BP, JVP, poor skin turgor

signs of renovascular disease- abdominal bruits, impalpable peripheral pulses

60
Q

examination of renal AKI

A

rash

uveitis

joint swelling

61
Q

examination of post-renal AKI

A

palpable bladder

62
Q

what investigations do you do in all patients with AKI

A

urine dipstick
monitor urine output
compare current renal function to historical records (if available)

63
Q

SALFORD for AKI management

A

S epsis and other causes to treat
A CE/ARB and NSAIDs suspend/review drugs
L abs (repeat creatinine within 24hrs) and L eaflets (for patients)
F luid assessment and response
O bstruction (USS should be performed within 24hrs in none-resolving AKI)
R renal/critical care referral
D ip urine and record it

64
Q

why is urine dipstick important in AKI

A

> 3+ proteinuria indicates intrinsic renal disease (send urine PCR/MSU if dipstick +ve)

65
Q

when would you start dialysis (renal replacement therapy RRT) in AKI

A

if any of the following are present and they are refractory to medical therapy:

hyperkalaemia
pulmonary oedema
severe metabolic acidosis
uraemia- uraemia pericarditis or encephalopathy
ingestion of certain toxins

66
Q

what is acute interstitial nephritis

A

often drug induced
clinical syndrome characterised by inflammatory infiltrates in renal interstitium (seen on renal biopsy) in response to drug, infection or autoimmune process

67
Q

what test without contrast can image the urinary tract

A

CTUKB
looks at kidneys ureters and bladder

68
Q

what is a USKUB

A

ultrasound of kidney, ureters and bladder

69
Q

when does kidney function return to normal again following AKI

A

within 3 months kidney function returns to baseline

70
Q

what does a high HR and low BP suggest

A

shock

71
Q

what is melaena

A

black smelly stools
digested blood which has been processed by the gut suggesting it is a bleed from the upper GI tract

72
Q

what are the 5 types of shock

A

hypovolemic
cardiogenic
disributive
obstructive
neurogenic

73
Q

what are the 4 categories of shock

A

fast- extreme tachycardia / bradycardia

fill- haemorrhage or dehydration so reduced BV

pump- primary cardiac problem (acute MI, aortic dissection, papillary muscle rupture) or something preventing the hearts ability to pump blood out of the thorax (tension pneumothorax, massive PE, cardiac tamponade)

squeeze- sepsis and anaphylaxis both involve capillary dysfunction which causes fluid from the blood vessels to leak out into the tissues

74
Q

what is shock

A

state that results when circulatory insufficiency leads to inadequate tissues perfusion and thus inadequate O2 delivery to tissues

the shortage of O2 means aerobic metabolism cannot occur thus resulting in organ dysfunction

75
Q

what signs tell you the circulatory system is working (adequate perfusion)

A

alert, normal mental state

warm and dry, CRT <2 seconds

urine output >30mL/Kg/Hr, urine looks clear or light yellow

HR 60-100

normal acid base balance, lactate being metabolised

76
Q

what signs suggest tissue hypo perfusion (circulatory system not working)

A

altered mental state

mottled, clammy skin

oliguria

tachycardia

elevated blood lactate

77
Q

causes of hypovolemic shock

A

haemorrhage
dehydration

78
Q

causes of disrubtive shock

A

sepsis
anaphylaxis

79
Q

causes of obstructive shock

A

PE
tension pneumothorax

80
Q

causes of cardiogenic shock

A

MI
arrhythmias
cardiac tamponade

81
Q

causes of neurogenic shock

A

cervical spinal cord injury

82
Q

what suggests hypovolaemic shock

A

signs of shock

evidence of bleeding/fluid loss

cool peripheries

good response to fluid or blood resuscitation

83
Q

what suggests distributive shock

A

signs of shock

peripheral vasodilation (warm dilated peripheries)

recent infection that has been getting worse (sepsis)

known exposure to allergen (anaphylaxis)

febrile (showing symptoms of fever)

may respond to fluids but if this is not the underlying cause patient may remain hypotensive

84
Q

what suggests obstructive shock

A

signs of shock

signs of problem in thorax which is impending CO

tension pneumothorax- respiratory distress, asymmetric chest expansion, dilated neck veins, tracheal deviation away from the affected side, absent breath sounds on affected side, hyper-resonant percussion not on affected side

cardiac tamponade- dilated neck veins, muffled heart sounds

massive PE- signs of shock plus signs of DVT or history suggestive of PE/VTE risk factors

85
Q

what suggests cardiogenic shock

A

will be suggested by the history

patient will usually have presented with adverse cardiac features- chest pain, syncope or signs of heart failure

cold peripheries

ECG may give clues

86
Q

what suggests neurogenic shock

A

this type of shock is a specific syndrome that happens in trauma (different to spinal shock)

happens in high (cervical or high thoracic) spinal cord injuries where the patient loses their sympathetic outflow hence their normal sympathetic responses to blood loss

instead of tachycardic they will be bradycardic

instead of hypotension and peripherally vasoconstricted/cold they will be hypotensive but peripherally dilated/warm

87
Q

what is the most common type of shock

A

sepsis (62%)
then hypovolaemic and cardiogenic (16%)

88
Q

what structure to use when handing over to a consultant about an acutely unwell patient

A

introduce- yourself

situation- patient (age and sex), what signs they have and what you suspect it is

background- how they came into hospital and why (the situation before), PMH and medications

assessment- how they look and observations, and examination findings and what you think the cause of these are

response- what you have done for the patient to manage, any investigations sent, anything you want to do and ask if there is anything else you can do

Semester 1 ( 3rd Year) (12 decks)

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