Basic Concepts of Fluid and Electrolyte Therapy

More documents

Recommendations

Info

AKI is most commonly secondary to a combination of sepsis and hypovolaemia, which results in hypoperfusion of the kidneys and prerenal AKI. Failure to correct the hypoperfusion may result in the development of acute tubular injury and intrinsic AKI, classically referred to as acute tubular necrosis (ATN). However it is important to exclude other possible causes so that a rarer aetiology, e.g. vasculitis, is not overlooked (Table 20). Table 20: Classification and causes of AKI Pre-renal AKI Intrinsic AKI Post-renal AKI intravascular volume depletion fever vomiting diarrhoea burns shock (vasodilatation and hypoperfusion) cardiogenic shock septic shock anaphylactic shock decreased renal perfusion pressure renal artery stenosis/thrombosis congestive cardiac failure liver failure/cirrhosis nephrotic syndrome drugs NSAIDs angiotensinconverting enzyme inhibitors angiotensin receptor blockers tubular injury ischaemia/ reperfusion injury nephrotoxins aminoglycosides cisplatin intravenous iodinated contrast media myoglobin myeloma light chains glomerular glomerulonephritis interstitial interstitial nephritis drugs infections vascular atheroembolic disease cholesterol embolisation blocked urinary catheter retro peritoneal fibrosis kidney stones prostatic disease pelvic tumour renal vein thrombosis iatrogenic injury to both ureters 82
Clinical Features There should be a high index of suspicion for AKI, particularly in an acutely ill patient with risk factors. Information about the patient’s previous kidney function (e.g. serum creatinine), particularly over the preceding 3 months, is a vital part of the evaluation. As in every other clinical condition, diagnosis is achieved by weighing all the evidence derived from a full history, examination and appropriate investigations. Serial changes in clinical features are often more revealing than single measurements taken at any one time. AKI should be considered as part of the differential diagnosis in patients presenting with the following clinical features (Table 21). Table 21: Clinical features of patients with suspected AKI and recommended baseline investigations History Examination Investigations risk factors (Table 18) symptoms predisposing to hypovolaemia vomiting diarrhoea poor oral intake blood/plasma loss symptoms suspicious of vasculitis uveitis skin rash joint pains haemoptysis general weight temperature skin turgor (over clavicle) mucous membranes (misleading if mouth breathing) skin rash (vasculitis) joint swelling (vasculitis) uveitis (vasculitis) full blood count (FBC) urea and electrolytes (U&Es), including chloride and bi carbonate acid-base status (from arterial or venous blood gas analysis) liver function tests (LFTs) calcium and phosphate urinalysis (prior to urinary catheter) ultrasound of renal tract within 24 hours if obstruction suspected 83
Page 1 and 2:
Dileep N. Lobo Andrew J. P. Lewingt
Page 3 and 4:
Basic Concepts of Fluid and Electro
Page 5 and 6:
Foreword This book, ‘Basic Concep
Page 7:
Table of Contents 1. Normal Physiol
Page 10 and 11:
ever, contains large anions such as
Page 12 and 13:
Oral intake 1.5-2 L Saliva 1.5 L Ga
Page 14 and 15:
Table 2: Normal maintenance require
Page 16 and 17:
Kidney: this is the main organ for
Page 18 and 19:
Conversely, if the intake of Na + i
Page 20 and 21:
volume at all costs. It also explai
Page 22 and 23:
Conclusion Appropriate fluid therap
Page 24 and 25:
Intravascular fluid volume - the to
Page 26 and 27:
Colloid - a fluid consisting of mic
Page 28 and 29:
Base excess - Base excess is define
Page 30 and 31:
Parameter Urine output Significance
Page 32 and 33: Figure 5: Example of a vital signs
Page 34 and 35: Fluid balance charts These provide
Page 36 and 37: Osmolality In the presence of AKI,
Page 38 and 39: Chloride Despite the fact that seru
Page 41 and 42: 4. Properties of Intravenous Crysta
Page 43 and 44: 6-12 h. The colloid should be metab
Page 45 and 46: Table 8: Advantages and disadvantag
Page 47: Plasma- Sterofundin 0.18% Plasma-Ly
Page 50 and 51: 50 Patients receiving artificial nu
Page 52 and 53: Once resuscitation has been achieve
Page 54 and 55: (3) The answer to this question is
Page 57 and 58: 6. Methods of Fluid Administration
Page 59 and 60: Central Modern single or multi lume
Page 61 and 62: 7. Acid-Base Balance Introduction M
Page 63 and 64: vide a simple description of the mo
Page 65 and 66: change in Pco 2 = respiratory proce
Page 67 and 68: Table 15: Causes of metabolic acido
Page 69 and 70: Renal HCO 3 - loss results from re
Page 71: Mixed acid-base disorders These are
Page 74 and 75: Urine output should be interpreted
Page 76 and 77: assess clinical response to fluid i
Page 78 and 79: Oliguria following surgery 48 h and
Page 80 and 81: Definition AKI is a result of a rap
Page 84 and 85: History Examination Investigations
Page 86 and 87: Management Prevention Any patient a
Page 88 and 89: if no clinical response and no pulm
Page 90 and 91: acidosis pH 7.2-7.4 - there is ver
Page 92 and 93: Referral to nephrologist NOT all p
Page 94 and 95: Follow up Acute kidney injury is a
Page 96 and 97: DKA and HONK represent the two extr
Page 98 and 99: Fluids and insulin In the absence
Page 100 and 101: Surgery in the patient with diabete
Page 102 and 103: 10 mmol/l/day. In the differential
Page 104 and 105: portionately more water is lost tha
Page 106 and 107: Hypokalaemia: a fall in serum conce
Page 108 and 109: Four common aspects of Ca 2+ disord
Page 110 and 111: Treatment depends on severity and c
Page 112 and 113: 112
Page 114 and 115: Hypophosphataemia
Page 116 and 117: 116
Page 118 and 119: Prolonged periods of preoperative f
Page 120 and 121: position to postoperative parotitis
Page 122 and 123: 13. *Chowdhury AH, Lobo DN. Fluids
Page 124 and 125: 42. Hussein H, Lewington A, Kanagas
Page 126 and 127: 67. *Michell AR. Diuresis and diarr
Page 128 and 129: 94. *Stewart PA. Modern quantitativ
Page 130 and 131: colloids 7, 26, 41, 42, 43 44, 45,
Page 132 and 133:
intravascular compartment 20, 41, 4
Page 134 and 135:
Stewart approach 63, 71 sympathetic
Page 136:
Dileep N. Lobo Andrew J. P. Lewingt
show all

Basic Concepts of Fluid and Electrolyte Therapy

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?