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Advanced Clinical Nursing Theory > Acute Abdomen > Flashcards

Acute Abdomen Flashcards

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1
Q

define acute abdomen

A

any intra-abdominal disease process that leads to an acute onset of clinical signs

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2
Q
A
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3
Q

define acute abdomen

A

any intra abdominal disease process that leads to an acute onset of clinical signs

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4
Q

what is acute abdomen usually caused by?

A

inflammation of an organ
leakage of fluid from a damaged organ
entrapment of an organ

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5
Q

what are the clinical signs of an acute abdomen?

A

Increased RR and effort
increased HR
thready or poor PQ
pale and tacky MM with prolongued CRT or injected MM and rapid CRT
hypotension
hypothermic
collapsed or obtunded
hypersalivation and nausea
regurgitation
retching
vomiting
abdominal pain
distended abdomen
arrhythmias

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6
Q

what is indicated by pale and tacky MM and prolonged CRT?

A

hypovolaemia

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7
Q

what is indicated by injected (red) MM and rapid CRT?

A

sepsis

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8
Q

what may help to guide possible causes of abdominal pain?

A

sex
neuter status
breed - deep chested/large dogs

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9
Q

what are the main gastric causes of an acute abdomen?

A

GDV
FB
gastric ulceration or perforation
intussusception

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10
Q

what are the main abdominal causes of an acute abdomen?

A

septic peritonitis
blunt or penetrating abdominal trauma
mesenteric volulus

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11
Q

what are the main hepatic / pancreatic causes of an acute abdomen?

A

acute hepatitis
biliary obstruction or rupture
neoplasia
pancreatitis
splenic mass or torsion

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12
Q

what may be caused by a splenic mass?

A

haemoabdomen following rupture

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13
Q

what are the urogenital causes of an acute abdomen?

A

AKI
pylonephritis
urethral tear
uroabdomen
pyometra
prostatitis

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14
Q

what are the key signs of GDV?

A

retching and unproductive vomiting
hypersalivation

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15
Q

what occurs during GDV?

A

stomach dilates and rotates or twists

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16
Q

is GDV an emergency

A

obvs you idiot
life threatening
high risk of mortality

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17
Q

what can be seen following GDV if left for 2+ hours?

A

necrosis and septic peritonitis due to leakage of necrotic fluid

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18
Q

how is necrosis caused by GDV?

A

reduction in blood flow to GI tract and spleen

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19
Q

what type of shock is very commonly seen with GDV?

A

hypovolaemic

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20
Q

what CV effects are seen with GDV?

A

reduced cardiac output
systemic hypotension

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21
Q

why does GDV result in reduced cardiac output and systemic hypotension?

A

reduced venous flow due to compression of the vena cava by distended stomach

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22
Q

why are GDV patients in shock?

A

severely hypoperfused

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23
Q

what types of shock can be seen with GDV?

A

all 4
distributive
hypovolaemic
cardiogenic
obstructive

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24
Q

why are GDV patients in hypovolaemic shock?

A

reduced circulating volume leading to reduced venous return and so reduced SV and CO

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25
Q

why are GDV patients in distributive shock?

A

cytokine release causes vasodilation
this leads to leaky vessels and activation of coagulation
reduced venous return and so reduced SV and CO

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26
Q

what can distributive shock lead to?

A

SIRS and sepsis

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27
Q

what does SIRS stand for?

A

systemic inflammatory response syndrome

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28
Q

what is indicated by a GDV patient with SIRS or sepsis?

A

poor prognosis

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29
Q

why are GDV patients in cardiogenic shock?

A

reduction in venous return so reduced preload
stomach applies pressure to heart and lungs
reduction in contractility and so CO

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30
Q

why are GDV patients in obstructive shock

A

physical impediment of blood flow in vessels as they are collapsed due to the pressure from the stomach
reduced venous return and so SV/CO

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31
Q

what is the overall effect of all types of shock?

A

reduction in CO leading to poor perfusion and hypoxaemia

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32
Q

what is involved in stabilisation of GDV patients?

A

O2
IV
analgesia
IVFT
bloods
may need catecholamines
regular TPR and reevaluation
recording on hospital sheet

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33
Q

what is critical about IV placement in GDV patients?

A

as big as possible and preferably 2
no saphenous unless desperate

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34
Q

why are IVs in saphenous veins less useful in patients with shock?

A

peripheral vasoconstriction means reduction in perfusion of HL
drugs take longer to ave effect / reach site of action

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35
Q

what are the analgesia considerations for GDV patients?

A

opioids
avoid NSAIDs due to risk of AKI and gastic ulceration

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36
Q

what fluids can be used for fluid resuscitation?

A

hartmanns fine
hypertonic also ok for initial bolus

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37
Q

what is the main Hartmanns does range for fluid resuscitation?

A

20 ml/kg boluses
up to 80 ml/kg total

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38
Q

what is the consideration if hypertonic saline used?

A

less needed but fluid must be replaced with isotonic as soon as possible

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39
Q

how could hypertonic saline be included into fluid rescusitation?

A

initial dose with hypertonic
isotonic from then on

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40
Q

what patients is hypertonic saline not appropriate in?

A

dehydrated as will remove even more fluid from the tissues and worsen signs

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41
Q

what type of blood sample is ideal for GDV patients?

A

arterial

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42
Q

what analysis will be performed on blood samples of GDV patients?

A

blood gas
blood type
coags
PCV and TS
lactate
urea:creatinine

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43
Q

what is indicated by PCV and TS?

A

dehydration (increased PCV if deh)

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44
Q

what is indicated by lactate levels?

A

prognosis
high levels show high level of anaerobic activity

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45
Q

why may catecholamines be used in GDV patients?

A

increase vascular resistance and so cardiac output

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46
Q

what is seen on a GDV xray?

A

pylorus cranial and dorsal

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47
Q

what is US used for in GDV assessment?

A

POCUS for gas filled space or haemoabdomen

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48
Q

what is xray used for in GDV assessment?

A

confirmation of GD or GDV
assessment of thorax for aspiration pneumonia

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49
Q

why may GDV patients be at risk of aspiration pneumonia?

A

regurgitation

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50
Q

what must be done before gastric decompression begins?

A

fluid rescusitation must be underway

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51
Q

what is the aim of gastric decompression?

A

removal of fluid and gas from the stomach

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52
Q

what can happen to the patient as the stomach is decompressed?

A

become more ‘shocky’

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53
Q

why may patients become more ‘shocky’ as the stomach is decompressed?

A

sudden toxin release as pressure is reduced and blood flow is normalised

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54
Q

what can be caused by sudden toxin release following gastric decompression?

A

SIRS
sepsis

55
Q

what is SIRS?

A

exaggerated defense response of the body to a noxious stressor

56
Q

how do SIRS and sepsis differ?

A

sepsis is SIRS which has a known infectious cause
can have SIRS without sepsis but nor sepsis without SIRS

57
Q

what are the main ways of decompressing the stomach?

A

percutaneous
oro-gastric

58
Q

what is involved in percutaneous gastric decompression?

A

insertion of large catheter into area where stomach is most distended in order to release air

59
Q

what is involved in oro-gastric gastric decompression?

A

stomach tube placed once patient under GA
tube held as low as possible to allow contents to escape

60
Q

what should you do if resistance is felt which the stomach tube is being advanced?

A

stop passing the tube

61
Q

how rapidly will patients be taken to surgery for GDV?

A

depends on patient
some may be stabilised more before
others will have only a short period of stabilisation

62
Q

what is needed in theatre for GDV surgery?

A

crash kit
flush
stomach tubes
suction unit
warm fluids for lavage
monitoring equipment
large surgical kit
spare kit
self retaining retractors
table which will tilt or trough
scrub nurse
circulating nurse

63
Q

what may be done with crash drugs before GDV surgery?

A

calculated and drawn up

64
Q

what are the main anaesthesia considerations for GDV patients?

A

hypotension
hypoxia
hypoxaemia
metabolic acidosis
hypothermia
arrhythmias
regurge

65
Q

what is hypoxia?

A

low O2 in body tissues

66
Q

what is hypoxaemia?

A

low O2 in blood

67
Q

what tests may indicate metabolic acidosis?

A

lactate
acid base
base excess

68
Q

what may be used to correct metabolic acidosis?

A

spiked fluids

69
Q

how can risk of regurge be managed?

A

head up induction
prophylactic gastro protectants
cuff ET tube
have suction ready
regular checking of ET tube cuff

70
Q

what arrhythmias are commonly seen with GDV?

A

VPCs
VT

71
Q

how many VPCs in a row indicate VT?

A

4 or more

72
Q

what treatment would be started if more than 4 VPCs were seen in a row?

A

lidocaine bolus
then CRI

73
Q

what should be done with all GDV patients prior to induction?

A

pre-oxygenation

74
Q

what pre-med would be used for GDV patients?

A

opioid only

75
Q

why would the premed used for a GDV patient be opioid only?

A

ACP and dex/medetomidine cause too much CVS compromise

76
Q

what are the CVS effects of ACP?

A

vasodilation
need to assist patient to maintain BP anyway as shock

77
Q

what are the CVS effects of dex/medetomidine?

A

vasoconstriction - worsening of hypoperfusion

78
Q

what may influence choice of induction agent?

A

alfax can cause VT which may worsen arrhythmias

79
Q

what induction agent would be used for GDV patients?

A

co induction
midazolam and propofol or alfaxalone

80
Q

what is the aim of coinduction?

A

reduction of required induction agent

81
Q

how may patients with GDV be maintained?

A

iso/sevo
fentanyl CRI
local block

82
Q

what must be monitored in GDV patients post op?

A

BP

83
Q

what BP must patients be maintained at to ensure organ perfusion?

A

60 mmHg

84
Q

how may hypotension be treated?

A

volume related - IVFT
vagally mediated - anticholinergics

85
Q

what anticholinergics may be used for vagally mediated bradycardia?

A

atropine
glycopyrrolate

86
Q

what is vagally mediated bradycardia?

A

pressure on vagus nerve causes HR to drop in response which is inappropriate for patient condition

87
Q

what type of block is seen with profiund bradycardia?

A

AV block

88
Q

what level of bradycardia is atropine used for?

A

severe

89
Q

what level of bradycardia is glycopyrrolate used for?

A

milder (40-60 bpm)

90
Q

how long do patients need to be monitored for following GDV?

A

24-48 hours close monitoring

91
Q

what CVS signs can be caused by poor perfusion?

A

hypoxia and arrhythmias

92
Q

how can fluid status be assessed?

A

PCV
TS
MM
CRT
BP

93
Q

what is involved in post op monitoring of GDV patients?

A

HR
RR
MM
CRT
hydration
ECG
BP

94
Q

what analgesia may be used for GDV patients post op?

A

paracetamol
CRI

95
Q

how may nutrition be managed for GDV patients post op?

A

TTE
TPN
feeding tube

96
Q

what is normal UOP?

A

2ml/kg/hr

97
Q

what complications are you looking for following GDV surgery?

A

sepsis
SIRS
DIC
aspiration pneumonia
peritonitis

98
Q

what signs may suggest sepsis, SIRS or DIC?

A

oedema
bleeding
sudden deterioration

99
Q

what is the chance of GDV recurrence without gastropexy?

A

70-80%

100
Q

what is the chance of GDV recurrence with gastropexy?

A

4-10%

101
Q

how can GDV be prevented?

A

owner education

102
Q

how can owners avoid GDV?

A

low stress
small, frequent meals
avoid wet and dry mix
go slow bowls
prophylactic gastropexy

103
Q

what temperature may suggest sepsis in dogs?

A

<37.2
>39.4

104
Q

what temperature may suggest sepsis in cats?

A

<37.2
>39.4

105
Q

what HR may suggest sepsis in dogs?

A

> 120

106
Q

what HR may suggest sepsis in cats?

A

<140
>220

107
Q

what RR may suggest sepsis in cats?

A

> 40

108
Q

what RR may suggest sepsis in dogs?

A

> 24

109
Q

what WBC count may suggest sepsis in cats?

A

<6
>20

110
Q

what WBC count may suggest sepsis in dogs?

A

<6
>16
10% banded neutrophils

111
Q

what is sepsis?

A

release of chemicals (cytokines) into the blood stream to fight infection
inappropriate and unregulated response to these chemicals triggers changes which damage MOS

112
Q

how is sepsis caused by release of chemicals (cytokines) into the blood stream?

A

inappropriate and unregulated response leading to organ damage

113
Q

what samples should be collected from patients with oedema/suspected sepsis?

A

culture and sensitivity

114
Q

if sepsis is suspected how should patients be treated?

A

broad spectrum antibiotics until culture back
then targeted

115
Q

what is the benefit of starting antibiotics early if patients have sepsis?

A

reduction in risk of endotoxaemia

116
Q

what is haemoabdomen?

A

accumulation of blood within peritoneal cavity

117
Q

what animals is haemoabdomen more common in?

A

dogs

118
Q

what can haemoabdomen be caused by?

A

trauma
spontaneous (splenic mass rupture)

119
Q

how will patients with acute haemoabdomen present?

A

collapsed
hypovolaemia

120
Q

how will patients with chronic haemoabdomen present?

A

lethargy and aneamia

121
Q

what is PCV and TS like in acute haemoabdomen patients?

A

normal
will then drop when they are rehydrated

122
Q

what other blood factors may have been affected by bleeding?

A

clotting factors

123
Q

what treatment may haemoabdomen patients need?

A

blood transfusion

124
Q

what is uroabdomen associated with?

A

rupture or leak within urinary tract caused by damage to the bladder or other area along the tract

125
Q

how will patients with uroabdomen present?

A

collapsed
hypovolaemic

126
Q

what is the most common electrolyte imbalance seen with uroabdomen patients?

A

hyperkalaemia

127
Q

what can be caused by hyperkalaemia?

A

arrhythmias

128
Q

what is seen on EGC with hyperkalaemia?

A

spiked T waves

129
Q

how is hyperkalaemia treated?

A

IVFT with calcium for 20 mins
glucose or insulin CRI

130
Q

why are glucose or insulin CRIs used to manage hyperkalaemia?

A

force potassium back into cells and reduce blood conc

131
Q

what can cause metabolic acidosis in uroabdomen?

A

uraemic acids

132
Q

what can uraemic acids cause?

A

metabolic acidosis

133
Q

what injury can be associated with uroabdomen?

A

AKI

Advanced Clinical Nursing Theory (36 decks)

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