WK 7- Renal and Haematological Emergencies Flashcards
What are the functions of the kidneys
- Excretion of waste products
- Acid base homeostasis
- Osomolality homeostasis
- BP regulation→ ie. Renin angiotensin system
- Hormone synthesis/metabolism
What are some causes of pre-renal failure
- Hypovolemia
- Hypotension→ Cardiogenic shock, sepsis, anaphylaxis
- Reduced effective circulating volume→ Generalised oedema secondary to cardiac failure, liver failure, nephrotic syndrome
- Renal hypoperfusion→ Renal artery stenosis, hepatorenal syndrome
What does pre-renal failure mean
failure resulting from anything that impairs blood flow to kidneys
What are some complications of renal failure
CNS→ Altered LOC, confusion, seizures
CVS→ Dysrhythmias, fluid overload
GIT→ Stress ulceration, ileus
Haematological→ Anaemia, platelet dysfunction
Metabolic→ Hyperkalemia, hypocalcemia, metabolic acidosis
Immunological→ Infection, poor wound healing
What are some renal causes of renal failure
Vessels
→Large: renal artery thrombosis/embolism/dissection, renal vein thrombosis
→Small: vasculitis, malignant hypertension, thrombotic microangiopathy (HUS/TTP)
-Glomeruli: Glomerulonephritis
-Renal tubules→ Acute tubular necrosis- can be ischemic or Cytotoxic – pigments, drugs
-Renal interstitial tissue→ Acute tubulointerstitial nephritis
What are some causes of post-renal failure
Internal obstruction→ Stone, clot, casts, crystals
External–> compression→Prostatomegaly, tumour, haematoma
→ can be relieved by indwelling urinary catheter
How is acute renal failure managed
Treat reversible causes
- Pre-renal→ correct hypovolemia, hypotension, anaemia (give blood transfusion)
- Post-renal→ IDC, SPC or nephrostomy tube for higher obstruction
- Avoid secondary insults→ avoid non-steroidals, amino glycosides→ these worsen renal failure
- Maintain urine output
- Treat complications→Hyperkalemia Tx, Renal Replacement Therapy (haemodialysis for chronic renal failure patients)→ complications mainly occur chronic renal failure
- Specific treatment for underlying cause
What does hyperkalemia cause? How can it be fatal?
-Causes hyperpolarisation/repolarisation of the cell membrane leading to difficulty in initiating an action potential-> causes dysrhythmias (potentially life threatening), muscle weakness
What ECG changes are seen in a person with hyperkalemia
Peaked T wave, broad QRS, shortened PR, flat/or no P wave
-over time will become sinusoidal
How is hyperkalemia treated
-Stabilise cardiac membranes→ calcium gluconate 10ml→ give calcium only to pt with abnormal ECG or K+ greater than 7.5
-Shift K into cells→
-Nebulised salbutamol 20mg→ shifts K intracellularly
-IV actrapid (insulin)
-IV NaHCO3 100mmol
-Enhance elimination of potassium–>
PO/PR resonium 50g→ binds K in gut and creates osmotic gradient that pulls K out of the gut and excretes
-IV frusemide diuresis→ useful in fluid overload in pt
-Renal replacement therapy- Dialysis
What conditions lead to chronic renal failure
Diabetes, reflux neuropathy, -Glomerulonephritis, Polycystic kidneys, Renovascular, Predominantly renal causes
How is chronic renal failure managed
- Dialysis→ Haemo vs Peritoneal (can do at home→ flood the peritoneal with diasolate-> body will slowly calibrate on its own)
- Protein + fluid restriction
- BP control→ tend to be hypertensive, so are on multiple anti-hypertensives
- Supplements
- Ca, vit D, Fe, PO4 binders, multivitamins
- Erythropoietin→ stimulates RBC formation
What is haemostasis
-a constant process of clot formation and clot lysis→ so there is no abnormal thrombosis
What are the 3 processes of haemostasis
-Vasoconstriction, platelet plug formation and coagulation
What 3 factors contribute to abnormal bleeding
→vessel injury–> severing the vessel can cause haemorrhage (cannot be repaired via platelet plug)
→ platelets; thrombocytopenia, platelet dysfunction (ie. Aspirin/clopidogrel)
→ coagulation cascade; coagulopathy
What are the two ways in which a person can get coagulopathy
Congenital or acquired
How can coagulopathy be congenital
ie. inherited syndromes like haemophillia
How can coagulopathy be acquired
→Inadequate synthesis; Liver disease, vit K deficiency
→Coagulation inhibition; Antibodies, drugs (ie. Warfarin, novel oral anticoagulants)
→Coagulation factor consumption;
Disseminated intravascular coagulation, snakebite
How is major bleeding managed
Resuscitation→ DRABCD
-Early source control→ stopping the bleeding
→ Physcial measures: pressure (ie. Lower limb bleed-pressure on femoral artery), elevation, splinting- helps tamponade the bleeding and alleviates pain
→ Surgical haemostasis: damage control surgery → controlling bleeding and correcting haemodynamics initially
→ Specific medical treatment: eg- upper GI bleed= PPI+ octreotide, antivenom for snakebite (Binds to venom and stops progression of coagulopathy)
What is tranexamic acid
anti-fibrinolytic derivate of lysine that interferes with the normal fibrinolysis process and competitively inhibits activation of plasminogen through reversible interactions with lysine-binding sites on the enzyme
How does saline make coagulopathy worse in a major trauma
- dilutes clotting factors- prolonging haemorrhage
- has no oxygen carrying capacity-> further decreases perfusion to tissues