Critical care: GI Flashcards
What is a metabolic acidosis
Decrease in pH due to metabolic cause
What is the anion gap? how is it calculated? What is a normal anion gap?
-Difference between cations (+ve-cats are positive) and anions (-ve) in your blood
-(Na+ + K+) - (Cl- + HCO3-)
-Should be 8-16/ around 12
What is a high anion gap acidosis? What are the causes?
Increase in unmeasured anions: LKTR
Lactate
Ketones
Toxins (salicylates, metformin)
Renal failure (impairment of H+ excretion)
What are the causes of normal anion gap metabolic acidosis?
-Loss of bicarb, i.e. high bowel output
–> fistulas
–> stomas
–> diarrhoea
Too much Nacl
Renal tubular acidosis (kidneys excrete bicarb)
Bicarb is replaced by chloride which is also a buffer
Indications for RRT
Refractory uraemic encephalopathy
Refractory acidosis
Refractory fluid overload
Refractory hyperkalaemia
Toxins
Complications of dialysis
-Hypotension: losing fluid
-Electrolyte shift
-Coagulopathy: citrate chelates calcium –> cofactor –> stops clotting
-Complications from line: bleeding, damage to local structure, pneumothorax
Why is anion gap corrected for albumin? how is this done?
the normal AG = 0.2 x [albumin] (g/L) + 1.5 x [phosphate] (mmol/L)
Albumin is major unmeasured anion: changes in albumin levels can significantly change equation
Describe patholphysiology of NAGMA vs HAGMA
High anion gap metabolic acidosis: bicarb is consumed by unmeasured cation (e.g. h+) as a result of its action as a buffer–> high anion gap
normal anion gap metabolic acidosis: Loss of bicarb is primary pathology, gets replaced by Cl- (also a buffer): therefore is hyperchloraemic metabolic acidosis
What is dialysis
Countercurrent exchange between blood and dialysate, exchange accross semipermeable membrane
Molecules are removed via diffusion
What is haemofiltration
-Haemofiltration - fluid is driven across the
semipermeable membrane by convection (pressure gradient)
-The solutecontaining plasma water is removed from the body and replaced with clean fluid.
How would gastric outlet obstruction present?
-Projectile vomiting undigested food
-Early satiety
-Unintentional weight loss
-Bloating
What would differentials be for gastric outlet obstruction?
Large gastric polyp in antrum/pylorus
Peptic ulcer disease
Carcinoma of stomach/head of pancreas/duodenum
What are the causes of metabolic alkalosis?
-Persistent vomiting (loss of HCL, hypokalaemia, hyponatremia–> kidneys retain sodium at expense of H+ to preserve Na/K+ pumps, worsening alkalosis
-Contraction alkalosis: e.g. due to dehydration: aldosterone causes renal H+ excretion
-Use of loop diuretics and thiazides: loss of sodium and water causes contraction alkalosis
-Primary hyperaldosteronism (conn’s)
Explain the phenomenon of aciduria in gastric outlet obstruction
-Prolonged vomiting leads to loss of HCL and K+: hypochloraemic hypokalaemic metabolic alkalosis
-K+ is shifted from intracellular to extracellular compartment, depleting body’s store of K further
-As dehydration worsens, kidneys preferentially reabsorbs Na and water, over K+ and H+–> paradoxical aciduria
What are ecg changes with hypo and hypercalcaemia
Hyper: Short QT
Hypo: prolonged QT
What are ecg changes of hyper/hypokalaemia
Hypo: small/inverted t waves
U waves after t waves
Prolonged pr
ST depression
Hyper:
Tall tented t waves
Broad QRS
Flattened P wave
What do gastrin and pepsinogen do?
Gastrin: stimulates secretion of gastric acid
Pepsinogen: protein digesting enzyme. Converted to pepsin by hydrochloric acid
What hormones are produced and by which cell type in stomach?
G cells in pyloric antrum of stomach, duodenum and pancrease: Gastrin
Parietal cells: HCL and intrinsic factor
Pepsinogen: chief cells
In what syndrome is gastrin produced in excessive levels? What are its features?
Zollinger ellison syndrome (gastric acid hypersecretion, peptic ulceration, gastrinoma)
How would you diagnose and treat zollinger-ellison
Investigations:
-Secretin stimulation test–> measures evoked gastrin levels
-Fasting gastrin levels, on 3 separate occasions
-Increased level of chromogranin A (common marker neuroendocrine tumour)
Treatment
-PPI (omeprazole, lansoprazole)
-Octreotide (mimics somatostatin)
Surgery +/- chemotherapy
What would you find on examination of baby with congnital hypertrophic pyloric stenosis?
Dehydration
Olive shaped mass right upper quadrant/epigastrium
What would be your initial management of pyloric stenosis
NBM
NG tube
Fluid resuscitation, correct electrolytes
UO monitoring
Bloods + capillary blood gas
What investigations would you carry out to confirm diagnosis of pyloric stenosis?
US
Feeding test
What would be definitive management of pyloric stenosis?
Open/laparascopic pyloromyotomy
What are the functions of the spleen?
FISH
Filtration and removal of old/abnormal red cells/white cells/platelets
Immunological properties: antibody synthesis
Storage of platelets
Haematological properties: extramedullary erythropoiesis in adults, erythropoeisis in foetus
What is grade 1 splenic haematoma?
Subcapsular haematoma <10% surface area
Capsular laceration <1cm in depth
What is grade 2 splenic haematoma?
Subcapsular haematoma 10-50% surface area
Intraparenchymal haematoma <5cm in diameter
Laceration 1-3cm depth not involving trabecular vessels
What is grade 3 splenic haematoma?
Subcapsular haematoma >50% of surface area/expanding
Intraparenchymal haematoma >5cm or expanding
Laceration >3cm depth or involving trabecular vessels
Ruptured subcapsular/parenchymal haematoma
Grade 4 splenic haematoma
Laceration involving segmental/hilar vessels with major devascularisation (>25% spleen)
Grade 5 splenic haematoma
Shattered spleen: hilar vascular injury with devascularisation spleen
How would you classify splenic injury?
Grade 1-5
What are options for management of splenic injuries?
Isolated grade 1/2 splenic injury may be suitable for conservative management
Grade 3-5
-If haemodynamically unstable, early resuscitation and emergency surgery
-If haemodynamically stagble with signs of bleeding (dropping serial hb: consider IR/surgery
What specific problems may occur post splenectomy?
Severe infection following splenectomy by encapsulated organism
Strep pneumonia, haemophilus, neisseria meningitidis
Malaria parasites
Greatest risk during first 2 years, but persists throughout life
What measures would you consider in patients post splenectomy?
Haemophilus influenza type b vaccine
Meningococcal group c vaccine
Pneumococcal vaccine
Antibiotics for minimum 2 years, preferably lifelong (oral pen v/clarithromycin if pen allergic)
Children: until minimum age 16 (as well as minimum 2 years and preferebly lifelong)
What maintenance fluid would you use in children?
0.9% sodium chloride + 5% glucose
What type of fluid would you use for replacement of NG losses in children?
0.9% sodium chloride with 10mmol K
How would you calculate maintenance fluids in children?
4ml/kg for first 10kg
2ml/kg for next 10kg
1ml/kg for subsequent kgs
How would you give fluid bolus in child?
20ml/kg 0.9% saline
Causes of pancreatitis
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps and other viruses (epstein barr, cmv)
Autoimmune
Scorpion sting, snake bites
Hyperlipidaemia
ERCP
Drgus (steroids, NSAIDs, diuretics-furosemide and thiazides)
Glasgow criteria for pancreatitis
PaO2 <8
Age >55
Neutrophils (WCC) >15
Calcium <2
Renal (urea- >16
Enzymes (LDH > 600/AST >200)
Albumin <32
Sugar >10
> 2 = severe pancreatitis
What is a tips procedure?
Interventional radiology procedure which establishes communication between inflow portal vein and outflow hepatic vein
-Access via internal jugular vein
-Used to treat portal hypertension and varices
-Reduces blood pressure in portal venous system
What parameters are accounted for in classes of shock?
6 parameters
-Amount of blood lost
-Pulse
-Blood pressure
-Respiratory rate
-Urine output
-Mental state
Class 1 shock
<750ml blood loss
Pulse <100
bp normal
rr 14-20 ml
UO >30ml/hr
slightly anxious
Class 2 shock
750-1500 ml blood loss
Pulse 100-120
BP normal
RR 20-30
UO 20-30ml/hr
increasingly anxious
Class 3 shock
1500-2000 ml blood loss
Pulse 120-140
BP reduced
RR 30-40
UO 5-15ml/hr
Confused
Class 4 shock
> 2000 ml/hr
Pulse >140
BP reduced
RR >40
UO negligible
Drowsy
What blood products are avaiable for transfusion in shocked patient? How soon are these available?
Packed red cells (o negative: available immediately, type specific blood: available after 10 mins, cross matched blood available after 1 hr)
Platelets
FFP
1:1:1 ratio
What is the difference between ffp and cryoprecipitate?
-FFP: fluid portion of 1 unit blood that has been separated and frozen at -18 degrees within 6 hrs collection
-Used to reverse warfarin, in massive transfusion and to replace specific clotting factor deficiencies
Cyropreceipate: prepared from plasma. One unit is formed from 4-6 units of blood
-used in Bleeding from excessive anticoagulation, massive haemorrhage, von willebrand, haemophillia, DIC
-Composed of factor 8, factor 13,fibrinogen, von willebrand
Describe transfusion reactions
Immediate;
-Anaplylactic
-Febrile
Within 6 hours
-Trali: non cardiogenic pulmonary oedema due to activation of immune cells in lungs
-TACO: volume overload
Within 24 hrs
-Acute haemolytic reaction (chills, fever, hypotension, hyperbilirubinaemia)
> 24 hrs
-Graft versus host (rash, liver dysfunction, diarrhoea)
-Post transfusion purpura
4- 8 days
-Delayed haemolytic reaction
How would you reverse warfarin in an emergency?
Product would depend on inr and level of bleeding
-discuss with haematology
-Vitamin K and pcc if active bleeding
-FFP produces suboptimal anticoagulation: only if PCC unavailable
Define hypotheramia
Core body temperature <35 degrees
Which part of brain regulates temperature?
Anterior hypothalamus
What are signs of hypothermia?
Shivering
Change in HR
Change in RR
Altered GCS
Pallor
Cyanosis
Why is surgical pt at increased risk of hypothermia?
-General/regional anaesthesia causes loss of behavioural response to cold and impaired thermoregulatory heat preserving mechanisms
-Anaesthetic induced peripheral vasodilatation
-Use of un-warmed blood/iv fluids and cold anaesthetic gases
-Reduced metabolic activity
-Environmental factors (e.g. low theatre temp)
-Increased head loss - environmental exposure
What measures can be taken to minimise hypothermia intraoperatively?
-Maintain optimum ambient temp above 21 degrees
-Adequate/appropriate clothing
-Minimise exposure of operating field
-Warmed fluids/blood/anaesthetic gas
-Insulating drapes
-Warming blankets
-Bair hugger
What is the body’s response to hypothermia?
-Piloerection
-Vasoconstriction
-Increased basal metabolic rate (shivering thermogenesis)
-Increase metabolism (due to hyroid hormones and catecholamine-mediated ‘brown fat metabolism’ (non shivering thermogenesis)
-Behavioural e.g. moving to warm environment, wearing more layers of clothes, turning heating on
What are the physiological effects of hypothermia?
Respiratory
-Oxyhaemoglobin curve shifts to left
-non cardiogenic pulmonary oedema
Haematological
-Increased blood viscosity
-Coagulopathy
Renal
-Cold diuresis
-Immobilisation and rhabdomyelysis
Cardiac
-Arrhythmia
Systemic
-Sympathetic excitation
-Sympathetic excitation
-Oxyhaemoglobin curve shifts to left
-Cold diuresis
-Coagulopathy
-Increased blood viscosity
-Immobilisation
-arrythmias
-Non cardiogenic pulmonary oedema
-Sympathetic nervous system excitation (shivering, hypertension, tachycardia, tachypnoea, vasoconstriction)
-Cold diuresis (inability to concentrate urine due to renal cell dysfunction, decreased levels adh) –> leakage of fluid into interstitial tissues leading to hypovolaemia
-Confusion (neurons initially stimulated, but are then depressed)
-Immobilisation –> muscle necrosis, myoglobinuria, ATN
-Pulse and respiration decrease, major organs fail
-Oxyhaemoglobin curve shifts to left
-Haemoconcentration and inreased viscosity that can result in thrombotic and embolic complications
-Coagulopathy due to thrombocytopaenia, decreased tnzymatic actions
-non-cardiogenic pulmonary oedema
-Arrhythmias
What are the metabolic effects of hypothermia?
-Hyperglycaemia (decreased glucose consumption by cells; decreased insulin secretion; tissue sensitivity to insulin blunted; glucose released from liver).
-Hypoglycaemia (common in alcoholics as their glucose stores are depleted)
-Cellular metabolic processes shut down
-acidosis from carbon dioxide retention and lactic acidosis
What ecg changes might be expected in hypothermia?
-Sinus bradycardia
-Prolonged PR
-Prolonged QT
-‘J’ waves (extra deflection at end of QRS, just overlapping beginning of ST segment)
How would you manage mild hypothermia? What temperature classifies as mild?
32-34.9
-Passive rewarming
-Use of person’s own heat generating ability
-insulating dry clothing
-Warm environment
How would you manage moderate hypothermia? What temperature is moderate hypothermia defined at?
28-31.9
-Active external rewarming
-Warming devices externally e.g. bair hugger
How would you manage severe hypothermia?
20-27.9
-Active internal (core) rewarming
-Warmed IV fluids
-Warmed humidified inhaled air
-Irrigation of body cavities with warmed fluids
-Extracorporeal rewarming (e.g. heart lung machine-cardiopulmonary bypass
What are the stages of hypothermia?
Stage 1 is characterized by a person who is awake and shivering and is associated with a core body temperature of 32-35 degrees.
Stage 2 is characterized by a person who is drowsy and not shivering, their core temperature is typically 28 to 32 degrees.
Stage 3 features include being unconscious and not shivering with a core temperature of 20-28 degrees.
In stage 4 hypothermia the core temperature is less than 20 degrees centigrade and no vital signs are seen
Management of sepsis
Goal directed therapy with circulatory optimisation, with sepsis 6
What is the pathophysiology of hyperglycaemia in pancreatitis/
Destruction of beta cells in islets of langerhans
What is the pathophysiology of hypocalcaemia in pancreatitis?
Saponification of omental fat by released pancreatic enzymes. Released fatty acids chelate calcium, resulting in hypocalcaemia
What are the complications of pancreatitis?
Local complications
-Haemorrhage
-necrosis
-Pseudocyst
Systemic
-ARDS
-Metabolic effects (hyperglycaemia, hypocalcaemia)
-Ileus
-PV thrombosis
Sepsis
SIRS syndrome in the presence of an infection
Septic shock
Sepsis with hypotension refractory to fluid therapy
What are the principles of managing a pt with septic shock?
-Broad spectrum antibiotics, discussion with microbiologist
-Invasive cardiac monitoring and circulatory support - inotropes
-Ventilatory support - non-invasive ventilation (NIV) e.g. CPAP, intubation, ventilation
-Renal support - IV fluid resuscitation to ensure UO >0.5ml/kg/hr, haemofiltration, haemodialysis
-Nutritional support- enteral/parenteral nutrition
-Source control (surgical/radiological intervention)
-Consider higher level care
What is the natural progression of septic shock if not managed appropriately?
-Dysfunction in 2or more organ systems
-Potentially reversible
-Multi-organ failure (MOF)
-Multi-organ dysfunction syndrome (MODS) = clinical syndrome characterised by development of progressive and potentially reversible physiological dysfunction in 2 or more organs or organ systems induced by variety of acute insults including sepsis
What would be the expected mortality rate of a pateint who has developed SIRS/sepsis/severe sepsis/septic shock?
4 week mortality:
-SIRS 10%
-Sepsis 20%
-Severe sepsis 20-40%
-septic shock 40-60%
Define severe sepsis
Sepsis with organ dysfunction (Hypotension, oliguria, lactic acidosis, alteration in gcs)
What micro-organisms would you expect in pt with anastomotic leak?
E.coli
Bacteroides
Enterococcus
C.dif
Which antibiotics are beta lactams?
Penicilins
carbapenems
vancomycin
What is cryoprecipitate and how does it differ from PCC?
Cryoprecepitate is a frozen blood product prepared from plasma. One unit of cryo is formed from a pool of four to six units of blood instead of a single product. It is used to replace fibrinogen in patients who are at increased risk of bleeding.
PCC is combination medication of factors 2,7,9,10. Used primarily for rapid warfarin reversal prior to surgery or in those with bleeding. Trade names include beriplex.
