When beginning insulin therapy , care must be taken not to reduce the glucose levels too rapidly . The serum glucose concentration decline should be 2.7 – 5.5 mmol / l / hour . Should the levels decline more rapidly , significant complications can occur ( Battaglia & Steele , 2016 ). The brain produces small molecules that attract water , which maintains hydration of the brain when it is a hyperosmolar environment . These osmoles are not instantly removed when treatment has started , so rapid rehydration of the patient can occur , causing cerebral oedema , seizures , coma and death ( Battaglia & Steele , 2016 ).
Additional considerations
During DKA , the potassium will shift out of the cells into the serum to attempt to replenish renal losses and offset acid – base imbalances ( Battaglia & Steele , 2016 ). As a result , the patient will have a total-body depletion of potassium and will require potassium supplementation on arrival and throughout the treatment ( Table 4 ). During the treatment of DKA , potassium levels will continue to deplete due to dilution from aggressive fluid therapy , insulin-mediated uptake of potassium by the cells , correction of acidaemia and continued renal losses . To monitor potassium levels , they should be measured after initial fluid resuscitation and 6 – 8 hours after initiation of insulin therapy ( Battaglia & Steele , 2016 ). If , after continuous potassium supplementation has been administered , the patient remains hypokalaemic , it is recommended that magnesium levels are checked . If there is a depletion in magnesium , potassium levels will not normalise ( Battaglia & Steele , 2016 ).
Shifts in phosphorus will occur in the same way as potassium so , as the body is being treated for DKA , it will lose phosphorus and this will need to be replaced . Testing may not initially show hypophosphataemia as it is often most marked 1 – 2 days after initiation of insulin therapy , as phosphorus translocates into an intracellular location ( Boag , 2012 ). The patient will need to have the phosphate levels checked every 6 – 12 hours during the first 48 – 72 hours of treatment ( Boag , 2012 ).
Table 4 . Potassium supplementation requirements according to serum potassium ( VetsNow , 2013 ).
Serum potassium ( mmol / litre )
> 5.5 Do not add 4.1 – 5.4 20 3.1 – 4 30 2.6 – 3 40 2 – 2.5 60
Potassium chloride to be added ( mmol / litre fluids )
Hypophosphataemia will lead to intravascular haemolysis and supplementation will be required when plasma levels drop below 0.35 mmol / l ( VetsNow , 2013 ).
Intravenous bicarbonate therapy is controversial , as acidosis will mostly improve with insulin and fluid therapy alone as ketones are metabolised ( Battaglia & Steele , 2016 ). However , if the pH is < 7.1 and not showing an upward trend or responding to insulin administration , bicarbonate supplementation can be administered via CRI , providing it is possible to measure blood pH ( VetsNow , 2013 ). The dose of bicarbonate can be calculated as follows :
NaHCO 3 – ( mmol / l / hour ) = base deficit × 0.3 × weight ( kg )
Boag ( 2012 ) recommends giving one third to one half of this dose by slow intravenous infusion over 15 – 30 minutes . The acid – base status can then be reassessed on completion of the infusion . The remainder can then be added to the patient ' s fluids and given over a few hours , if necessary , while continuing to monitor acid – base and electrolyte status ( Boag , 2012 ). When the pH reaches 7.2 , the bicarbonate should immediately be stopped to prevent iatrogenic metabolic alkalosis ( Battaglia & Steele , 2016 ).
Nursing care
The role of the nurse in the care of a DKA patient is essential for an effective recovery . The patient is likely to be in a critical condition and will require almost continuous monitoring , whether that be recording vital signs or taking blood samples for glucose and electrolyte monitoring . Ideally , the patient will be placed in an intensive care facility with 24-hour nursing availability , as these patients are at a greater risk of deteriorating . Haskey ( 2015 ) discusses the use of a fourstep nursing process to maximise the care of the critical patient : assessment , planning , implementation and evaluation . The steps are used on a continuous cycle as often as needed . In more critical patients , where drug therapy response is key , this process may be used every 15 minutes .
One of the key vital signs to be monitored is the respiratory rate , as it will give an indication of the acidosis compensatory mechanisms . When the body goes into acidosis it has three mechanisms for compensation : buffers , respiratory compensation and renal compensation . When the respiratory system starts compensating for acidosis you can expect to see increased ventilation leading to decreased partial pressure of carbon dioxide . This increase in respiratory rate should not include an increase in respiratory effort and therefore dyspnoea should be viewed as a separate clinical sign . It will be common for the patient to have an increased respiratory rate on presentation and this
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