Case 8: An acutely unwell patient Flashcards
(88 cards)
1
Q
what is flank pain?
A
on the side of the back below the ribs and above the hips
2
Q
what could flank pain indicate?
A
kidney stones
infection
muscle strains
3
Q
what pathologies are relevant to the right hypochondrium abdominal quadrant?
A
acute hepatitis
biliary colic
cholangitis
cholecystitis
pneumonia (referred pain)
4
Q
what pathologies are relevant to left hypochondrium abdominal quadrant
A
splenomegaly
splenic abscess
splenic infarction
splenic rupture
pneumonia (referred pain)
5
Q
which pathologies are relevant to epigastrium abdominal quadrant
A
acute myocardial infarction
acute/chronic pancreatitis
gastroesophageal reflux disease
peptic ulcer
6
Q
which pathologies are relevant to right iliac fossa abdominal quadrant
A
appendicitis
hernias
renal calculi
7
Q
which pathologies are relevant to left iliac fossa abdominal quadrant
A
diverticulitis
hernias
renal calculi
8
Q
which pathologies are relevant to hypogastrium (suprapubic) abdominal region
A
bladder retention
cystitis
9
Q
what symptoms suggest upper urinary tract infection
A
acute colicky abdominal pain
dysuria
fever
vomting
10
Q
what symptoms suggest diverticulitis/gastroenteritis
A
new diarrhoea and vomiting
abdominal pain
fever
11
Q
which tool can screen for frailty
A
rockwood frailty score
scored 1-9
1= very fit
9= terminally ill
12
Q
why would you do a venous blood gas
A
for information on acid-base balance and lactate level
13
Q
what findings suggest sepsis
A
hypotension
tachycardia
pyrexia
mottled skin
reduced conscious level
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
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
16
Q
what is the end result of sepsis
A
tissue hypoxia
mitochondrial dysfunction
macrovascular and microvascular dysfunction
apoptosis
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
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
19
Q
source of sepsis in CNS
A
meningitis
encephalitis
cerebral/epidural abscesses
discitis
20
Q
respiratory sources of sepsis
A
pneumonia
lung abscess
21
Q
cardiac sources of sepsis
A
endocarditis
myocarditis
22
Q
skin/soft tissue sources of sepsis
A
cellulitis
infected bites/ulcers/wounds
necrotising fasciitis
23
Q
genitourinary sources of sepsis
A
pyelonephritis
cystitis
obstructed renal calculus
24
Q
GI sources of sepsis
A
gall bladder infections (cholecystitis, cholangitis)
diverticulitis
infective colitis
appendicitis
tonsilitis
25
orthopaedic sources of sepsis
septic arthritis
prosthetic joint infections
26
infected lines/devices sources of sepsis
peritoneal catheters
tunnel lines
central venous catheters
27
what fluid is given for sepsis
fluid resuscitation is with a crystalloid given as a bolus over less then 15 minutes
500mL of 0.9% Hartmanns solution
28
what are crystalloids
solutions containing small molecules of water
29
examples of crystalloids
sodium chloride
glucose
Hartmanns
30
what are colloids
solutions with large molecular weight molecules
31
examples of colloids
albumins
gelatins
32
why is lactate raised in sepsis
tissue hypoxia as a result of widespread systemic inflammation
there is organ hypo perfusion and subsequently cells turn to anaerobic metabolism which produces lactate
33
what might hyperkalaemia look like on ECG
tall tented T waves
broad QRS complexes (>0.12ms)
no discernible P waves
34
causes of hyperkalaemia
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)
35
when would you need to urgently treat hyperkalaemia
when serum K+ exceeds 6.5 and/or there are ECG changes
36
what are the priorities when treating hyperkalaemia
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
what should you do following administering each fluid in sepsis
repeat BP
38
what are the kidneys 3 main functions
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
what is a good marker for eGFR of kidneys
creatinine (waste product) as it is completely filtered in the glomerulus
40
what is the role of RAAS
increase blood pressure
it acts to increase the overall effective circulating volume by:
increasing reabsorption of Na+
and
vasoconstricting efferent arterioles
41
what causes acute tubular necrosis
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
does acute tubular necrosis have high mortality
yes at around 50% but it is usually to do with the associated illness such as septic shock
43
complications of AKI
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
what can the end effects of AKI be on other parts of body
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
why is clotting measured in sepsis patients
sepsis can be a cause of disseminated intravascular coagulation (DIC)
46
causes of disseminated intravascular coagulation (DIC)
sepsis
trauma
malignancy
obstetric complications (amniotic fluid embolism, placental abruption)
47
why does disseminated intravascular coagulation (DIC) happen
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
management of disseminated intravascular coagulation (DIC)
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
what is the definition of AKI
clinical syndrome characterised by an acute reduction in renal function leading to a rise in serum creatinine and/or decline in urine output
50
3 categorises of AKI causes
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
what is the most common cause of AKI
pre-renal= 85%
renal= 10%
post-renal= 5%
52
pre-renal causes of AKI
dehydration
sepsis
hypotension
shock
hepatorenal syndrome
severe heart failure
hypertension/compartment syndrome
53
renal causes of AKI
NSAIDs
ACEi
ARBs
gentamicin
GN/vasculitis
contrast
interstitial nephritis
myeloma
rhabdomyolysis
54
post-renal causes of AKI
prostatic enlargement
renal stones
pelvic cancer
55
risk factors for AKI
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
history of pre-renal AKI
poor oral intake/dehydration
diarrhoea or vomiting
57
history of renal AKI
fever, rash, joint pain, nasal crusting, weight loss
long lie history
NSAIDs use
nephrotoxic drug use
58
history of post-renal AKI
lower UTI symptoms in men
history of renal calculi (may cause hydronephrosis and obstruction)
59
examination of pre-renal AKI
signs of sepsis
slow cap refil, low BP, JVP, poor skin turgor
signs of renovascular disease- abdominal bruits, impalpable peripheral pulses
60
examination of renal AKI
rash
uveitis
joint swelling
61
examination of post-renal AKI
palpable bladder
62
what investigations do you do in all patients with AKI
urine dipstick
monitor urine output
compare current renal function to historical records (if available)
63
SALFORD for AKI management
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
why is urine dipstick important in AKI
>3+ proteinuria indicates intrinsic renal disease (send urine PCR/MSU if dipstick +ve)
65
when would you start dialysis (renal replacement therapy RRT) in AKI
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
what is acute interstitial nephritis
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
what test without contrast can image the urinary tract
CTUKB
looks at kidneys ureters and bladder
68
what is a USKUB
ultrasound of kidney, ureters and bladder
69
when does kidney function return to normal again following AKI
within 3 months kidney function returns to baseline
70
what does a high HR and low BP suggest
shock
71
what is melaena
black smelly stools
digested blood which has been processed by the gut suggesting it is a bleed from the upper GI tract
72
what are the 5 types of shock
hypovolemic
cardiogenic
disributive
obstructive
neurogenic
73
what are the 4 categories of shock
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
what is shock
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
what signs tell you the circulatory system is working (adequate perfusion)
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
what signs suggest tissue hypo perfusion (circulatory system not working)
altered mental state
mottled, clammy skin
oliguria
tachycardia
elevated blood lactate
77
causes of hypovolemic shock
haemorrhage
dehydration
78
causes of disrubtive shock
sepsis
anaphylaxis
79
causes of obstructive shock
PE
tension pneumothorax
80
causes of cardiogenic shock
MI
arrhythmias
cardiac tamponade
81
causes of neurogenic shock
cervical spinal cord injury
82
what suggests hypovolaemic shock
signs of shock
evidence of bleeding/fluid loss
cool peripheries
good response to fluid or blood resuscitation
83
what suggests distributive shock
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
what suggests obstructive shock
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
what suggests cardiogenic shock
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
what suggests neurogenic shock
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
what is the most common type of shock
sepsis (62%)
then hypovolaemic and cardiogenic (16%)
88
what structure to use when handing over to a consultant about an acutely unwell patient
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
