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L I Worthley

Publications and source records attributed to L I Worthley.

At least 19 recordsLinked to original sources
PubMed2001

Acid-base balance: part I. Physiology.

OBJECTIVE: To review the normal human acid-base physiology and the pathophysiology and management of acid-base disturbances in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts and a review of studies reported from 1990 to 2000 and identified through a MEDLINE search of the English language literature on acid-base balance. SUMMARY OF REVIEW: In a healthy individual the extracellular fluid pH change following addition of a metabolic acid or base, is modified initially by the body's buffers. Subsequent respiratory compensation, by excretion or retention of CO2, modifies this change before metabolism of the organic acid or renal excretion of the acid or alkali returns the plasma bicarbonate to normal. A primary respiratory acid base change is modified initially by cellular buffers, with renal compensatory mechanisms adjusting slowly to this change. However, correction of the respiratory pH disorder only occurs with correction of the primary disease process. CONCLUSIONS: In man the acid-base balance is maintained and regulated by the renal and respiratory systems, which modify the extracellular fluid pH by changing the bicarbonate pair (HCO3- and PCO2); all other body buffer systems adjust to the alterations in this pair.

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PubMed2001

Acid-base balance: part II. Pathophysiology.

OBJECTIVE: To review the normal human acid-base physiology and the pathophysiology and management of acid-base disturbances in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts and a review of studies reported from 1990 to 2000 and identified through a MEDLINE search of the English language literature on acid-base balance. SUMMARY OF REVIEW: Acid-base disorders are usually classified as metabolic (non-respiratory) or respiratory, depending on whether the primary change occurs in the plasma bicarbonate or the carbonic acid (i.e. carbon dioxide) concentrations, respectively. Respiratory or renal compensatory changes usually occur to minimise the effect of the primary disturbance. A metabolic acidosis arises from an abnormal process that generates non-carbonic acid or an abnormal loss of HCO3- and may be identified by an increase or normal anion gap, respectively. The arterial blood gas usually reveals a pH < 7.36, PCO2 < 35 mmHg and 'calculated' HCO3- < 18 mmol/L. In general, a high anion gap acidosis is managed by treating the disorder generating the acid (thereby ceasing the acid production) and enhancing the clearance of the acid anion (e.g. by metabolism or excretion) thereby regenerating the HCO3- reduced by buffering. A metabolic alkalosis arises from an abnormal process generating excess HCO3-. The arterial blood gas usually reveals a pH > 7.44, PCO2 > 45 mmHg and 'calculated' HCO3- > 32 mmol/L. As the kidney has a large capacity to excrete HCO3-, management usually requires treatment of the processes that are generating as well maintaining the alkalosis. Respiratory acidosis and alkalosis are usually caused by a primary disorder of carbon-dioxide excretion, and correction of the pH disorder only occurs with correction of the primary disease process. CONCLUSIONS: In man, acid-base disturbances are usually classified as either metabolic or respiratory. Correction of the underlying disorder is often all that is required to allow the body to metabolise or excrete the acid or alkali and return the buffer pair (HCO3- and PCO2) to normal.

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PubMed2001

Antiarrhythmic and haemodynamic effects of the commonly used intravenous electrolytes.

OBJECTIVE: To review the physiology and cardiovascular effects of the commonly used intravenous electrolytes. DATA SOURCES: Abstracts, articles and published reviews of studies reported from 1966 to 2000 and identified through a MEDLINE search on cardiac arrhythmias and electrolytes. SUMMARY OF REVIEW: While isotonic saline solutions are used to improve the haemodynamic status in critically ill patients who are hypotensive and hypovolaemic, other intravenous solutions including potassium chloride, calcium chloride, magnesium sulphate and sodium or potassium phosphate as well as hypertonic saline and sodium bicabonate have unique and often therapeutically useful haemodynamic and antiarrhythmic effects. Potassium chloride solutions are used to treat hypokalaemia with a maximum speed of correction in an adult of 20 mmol per 30 minutes when an acute myocardial infarct is present. A greater infusion rate may be necessary when ventricular or supraventricular tachyarrhythmias are present although close ECG monitoring will be required. Magnesium sulphate (2-20 mmol) has been used for hypomagnesaemic and normomagnesaemic cardiac arrhythmias (particularly when digoxin induced) and calcium chloride (3.4-6.8 mmol) is used to treat hyperkalaemic and hypermagnesaemic cardiac arrhythmias. Both hypertonic sodium bicarbonate and sodium chloride solutions have antiarrhythmic effects that may be beneficial in conditions that include tricyclic poisoning, hyperkalaemia and bupivicaine toxicity, although sodium bicarbonate is generally used for tricyclic cardiotoxicity. Low cardiac output states and arrhythmias have also been reported in hypophosphataemic patients that are reversed by infusions of potassium or sodium phosphate. CONCLUSIONS: Intravenous potassium chloride, calcium chloride, magnesium sulphate, sodium and potassium phosphate, sodium bicarbonate and hypertonic saline can be used effectively to alter the haemodynamic status and manage cardiac arrhythmias. However, their indications are selective and complications may occur, so careful administration and monitoring are required with their use.

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PubMed2001

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PubMed2001

Acute gastrointestinal bleeding: Part I.

OBJECTIVE: To review the management of acute gastrointestinal bleeding in the critically ill patient in a two part presentation. DATA SOURCES: Articles and a review of studies reported from 1991 to 2001 and identified through a MEDLINE search of the English language literature on acute gastrointestinal bleeding. SUMMARY OF REVIEW: Gastrointestinal bleeding is a relatively frequent problem in the critically ill patient. Common causes include acute stress ulceration (ASU), peptic ulceration and bleeding oesophageal varices. Non-variceal upper gastrointestinal bleeding requires resuscitation and correction of coagulation disturbances before endoscopy is performed. If a bleeding ulcer is detected it is often managed by an adrenaline injection or electrocautery into the base of the lesion and a proton pump inhibitor (e.g. omeprazole 80 mg i.v. followed by 8 mg/hr for 72 hr then 20 mg orally for 8 weeks). Surgery is considered for all patients in whom bleeding persists despite endoscopic or medical therapy. While H(2) receptor antagonists have been used for the management of ASU, proton pump inhibitors are currently prescribed due to their greater gastric acid suppressant effect (e.g. omeprazole 40 mg i.v. daily for ASU prophylaxis, 40 mg daily or 12-hourly for ASU with mild blood loss and 80 mg i.v. followed by 8 mg/hr for 72 hrs for ASU with severe haemorrhage). With severe haemorrhage, fibrinolytic inhibitors (e.g. tranexamic acid 3-6 g i.v. daily) may also be of benefit. For lower gastrointestinal bleeding or if there is no obvious upper gastrointestinal lesion during endoscopy, then selective mesenteric angiography with embolisation of the bleeding point (if the bleeding is brisk, e.g. > 0.5-2.0 mL/min) or colonoscopy with electrocautery or adrenaline injection (for diverticular haemorrhage) may be considered as an alternative to surgery. CONCLUSIONS: Acute upper gastrointestinal bleeding is often managed by intravenous proton pump inhibitors and endoscopy with electrocautery or adrenaline injection when a bleeding at the base of an ulcer is found. For lower gastrointestinal haemorrhage, selective mesenteric angiography with embolisation of the bleeding point is an alternative to surgery in critically ill patients. Fibrinolytic inhibitors may have added benefit.

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PubMed2001

Acute gastrointestinal bleeding: Part II.

OBJECTIVE: To review the management of acute gastrointestinal bleeding in the critically ill patient in a two part presentation. DATA SOURCES: Articles and a review of studies reported from 1991 to 2001 and identified through a MEDLINE search of the English language literature on acute gastrointestinal bleeding. SUMMARY OF REVIEW: Oesophageal varices are a common source of upper gastrointestinal bleeding in patients who have portal hypertension. Management requires resuscitation and treatment of associated coagulation disturbances along with intravenous octreotide (50 microg followed by 50 microg/hr for 48 hr) before endoscopy is performed. Octreotide is more effective than vasopressin in controlling acute variceal suppressant and has fewer side effects compared with glypressin. To provide haemostasis, endoscopic variceal sclerosis has largely been replaced by variceal ligation using an overtube and small elastic 'o' rings to band the bleeding variceal channels. If bleeding continues then Balloon tamponade and intravenous fibrinolytic inhibitors (e.g. tranexamic acid 3-6 g i.v. daily) are used for 24 hr before endoscopy (with variceal ligation) is repeated. If the variceal bleeding is resistant to repeated banding, portal decompression using transjugular intrahepatic portosystemic shunt or surgical shunt should be considered. While beta adrenergic blockers (e.g. propranalol) are indicated to reduce the incidence of rebleeding, they are contraindicated in a patient with actively bleeding oesophageal varices. CONCLUSIONS: Acute oesophageal variceal bleeding can often be managed successfully using octreotide and variceal ligation. If bleeding continues then transjugular intrahepatic portosystemic shunt or surgical shunt should be considered.

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PubMed2000

Induced and accidental hypothermia.

OBJECTIVE: To review human thermoregulation and the pathophysiology and management of induced and accidental hypothermia. DATA SOURCES: A review of studies reported over ten years from 1990 to 2000 and identified through a MEDLINE search of the English-language literature on thermoregulation and induced and accidental hypothermia. SUMMARY OF REVIEW: Hypothermia is defined as a core temperature less than 35 degrees C, and may be therapeutic (i.e. induced for clinical benefit) or accidental. Hypothermia induced prior to cardiovascular or neurosurgical procedures (i.e. therapeutic hypothermia) allows for a greater hypotensive operative period with less risk of cerebral or cardiac ischaemic injury. Hypothermia induced following tissue injury (e.g. closed head injury, cerebrovascular accident, adult respiratory distress syndrome) has also been used to reduce ischaemic tissue injury, although significant clinical benefits have not yet been demonstrated. Inadvertent hypothermia (i.e. accidental hypothermia) is classed as mild from 33 degrees C-35 degrees C, moderate from 30 degrees C-33 degrees C and severe if less than 30 degrees C. Treatment includes surface and core warming methods, all of which have a valid basis from experimental studies. However, no prospective, randomised controlled clinical trials exist that have compared the various rewarming methods. Currently, passive rewarming methods (e.g. reflective metalloplastic sheets, blankets) are recommended for patients with mild hypothermia (> 33 degrees C), active surface rewarming (e.g. heated blankets, hot air circulators) for moderate hypothermia (> 30 degrees C), active core rewarming (e.g. heated haemodialysis, haemodiafiltration or peritoneal dialysis) for severe hypothermia (< 30 degrees C), and heated cardiopulmonary bypass for severe hypothermia with cardiopulmonary arrest. CONCLUSIONS: Operative hypothermia reduces ischaemic injury during cardiac and neurosurgical procedures. Hypothermia induced following tissue injury has not yet been shown to be of benefit. Management of accidental hypothermia requires passive and active warming methods, the indication of each depending on the availability of the method and severity of hypothermia.

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PubMed2000

Shock: a review of pathophysiology and management. Part I.

OBJECTIVE: To review pathophysiology and management of hypovolaemic, cardiogenic and septic shock in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts and a review of studies reported from 1994 to 1998 and identified through a MEDLINE search of the English language literature on septic shock, cardiogenic shock and hypovolaemic shock. SUMMARY OF REVIEW: Shock is a clinical syndrome characterised by hypotension (i.e. a systolic blood pressure less than 90 mmHg or a mean arterial pressure less than 60 mmHg or reduced by greater than 30%, for at least 30 minutes), oliguria (i.e. a urine output less than 20 mL/hr or 0.3 ml/kg/hr for 2 consecutive hours), and poor peripheral perfusion (e.g. cool and clammy skin which demonstrates poor capillary refill). Hypovolaemic and cardiogenic shock are associated with disorders that cause an under-lying haemodynamic defect of a low intravascular volume and a reduction in myocardial contractility, respectively. The understanding and management of hypovolaemic shock has changed very little over the past 50 years with treatment requiring management of the causative lesion (i.e. surgical correction of blood loss) and replacement of the intravascular volume by infusing blood and/or 0.9% sodium containing colloid or crystalloid fluids. Due to recent developments in percutaneous coronary revascularisation techniques, management of cardiogenic shock in some centers has changed. Emergency cardiac catheterisation with urgent myocardial reperfusion (using percutaneous transluminal coronary angioplasty or coronary artery stenting in selected cases) and use of glycoprotein IIb/IIIa antagonists while supporting the circulation using an intra-aortic Balloon pump, has been reported to reduce mortality of cardiogenic shock in acute myocardial infarction. Large randomised, controlled multicentre trials are awaited. CONCLUSIONS: Hypovolaemic shock requires urgent management of the underlying defect and replacement of the intravascular volume loss. Recent studies in management of cardiogenic shock using urgent revascularisation and intra-aortic Balloon counterpulsation in patients with acute myocardial infarction have shown a reduction in mortality in selected cases.

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PubMed2000

Shock: a review of pathophysiology and management. Part II.

OBJECTIVE: To review pathophysiology and management of hypovolaemic, cardiogenic and septic shock in a two part presentation. DATA SOURCES: Articles and published peer-review abstracts and a review of studies reported from 1994 to 1998 and identified through a MEDLINE search of the English language literature on septic shock, cardiogenic shock and hypovolaemic shock. SUMMARY OF REVIEW: The pathophysiological effects of cardiogenic and hypovolaemic shock are related predominantly to a reduction in preload and myocardial contractility, respectively, whereas the pathophysiological effects of septic shock result largely from the overwhelming production of inflammatory mediators. The excessive inflammatory response results in haemodynamic compromise and widespread tissue injury. While the understanding of the acute inflammatory reaction has improved, therapies to modulate the chemical mediators responsible for the organ dysfunction associated with this reaction have not altered mortality, and in some instances may have increased it. Treatment of septic shock is still largely supportive, using intravenous fluids and inotropic agents to provide adequate tissue perfusion while the infective lesion is managed with antibiotic therapy and surgical drainage of septic focus. CONCLUSIONS: Septic shock is provoked by an excessive acute inflammatory response to an infection. Management of the shock is supportive using fluids and inotropic agents, while antibiotic therapy and surgical drainage of the septic focus take effect. Immunomodulation of the acute inflammatory response causing septic shock has not improved mortality.

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