DKA nursing assessment -
Insulin is required to help move glucose into the cells. And this fat breakdown leads to ketones building up in the blood, which are acids. During type 2 diabetes, the cells become resistant to insulin.
This is pretty rare, though. DKA mostly happens in type 1 diabetes. I just made them up to make learning all of this easier.
Step 1 of the pathophysiology of diabetic ketoacidosis is there is not enough insulin. And this leads to hyperglycemia, which is of the pathophysiology of DKA. So the cells are there really wanting their glucose, because they need energy.
But thankfully, they have some stored up fat to use for energy, and this is of DKA, the cells use fat as energy. This is step 4, ketones are produced as a biproduct of fat metabolism.
This is a key point to remember for DKA: the cells use FAT for energy instead of glucose. And when fat is broken down, ketones are released, and ketones are ACIDS. The more the ketone levels rise in the body, the more the acid level rises in the body, because ketones are acids.
And so the more ketones there are, the more serious the acidosis becomes. And this is considered metabolic acidosis. In that video, I walk you through what it is, and what causes it, so you will definitely want to check it out!
There are several nursing interventions you might do for a patient with DKA. These might be things like: giving fluids, giving insulin, and continuing to assess them. And, actually, that reminds me, I have a free nursing assessment cheat sheet for you. So it literally walks you through the nursing assessment word-for-word, so you can use it as a guide when you practice assessing a patient.
Normal saline or lactated ringers is usually given first because these solutions are isotonic, meaning they are not going to force fluid any which way.
Those solutions are going to stay inside the blood vessels, which is where we want them. As a result, the insulin is not there on the surface of the cell, like a bouncer, allowing glucose into the cell. Therefore, glucose is going to build up in that bloodstream, as we've already mentioned, resulting in hyperglycemia.
We got that. If we have no insulin allowing glucose into the cell and we have excess glucose building up in the bloodstream, instead of going to the cell, it's building up in the bloodstream, how does our brain interpret this, right?
How's our brain interpreting this? Well, our brain is thinking, why the heck are these cells not getting glucose, right? Why is there no glucose in these cells? Basically, the brain is saying our cells are being starved of glucose although we have hyperglycemia. Although we have an extreme excess amount of glucose in our blood, we're not getting that glucose into those cells where it needs to go.
The brain says, wait a minute, our cells are starving for glucose, they need more glucose. And so what does the body do to compensate? It attempts to release more glucose. It's saying, Hey, we don't have, we must not have, enough glucose in our blood. Let's release more so that these starving cells can get the glucose they need.
And how does our body release the glucose from those glycogen storages, remember, it does it through glycogenolysis right? The actual breakdown of those glycogen storages. So what occurs, as I mentioned in the previous slide, we're going to break down the glycogen reserves in the liver.
We're also going to break down the glycogen reserves in those fatty cells. Now, the problem is, whenever we actually break down one of these fatty cells where glycogen is being stored, sure, we're going to release glucose, right? That's what our brain is telling our body to do. A by-product of the glycogenolysis that occurs in these fatty cells is the release of ketones as well.
Now, similar to CO2, if you have seen that video, CO2 is an acid. So are ketones, they are also an acid. This is important. As we mentioned in our ABGs video, we have a very narrow pH range, a normal pH range of 7. If we have an excess of release of ketones into the blood, this is going to drive our pH to become more acidic, therefore becoming less than 7.
And we will recall from our ABGs video that because that range is so narrow, any alterations going below 7. It's incredibly problematic in patients. And this is what the entire issue with the cascade of symptoms with diabetic ketoacidosis is.
Again, we have too much blood glucose in our blood because we don't have insulin. It can't get to the cells. The cells are starving. The brain says, Hey, our cells are starving, we need to release more blood glucose. Glycogenolysis occurs.
The release of glucose occurs leading to further hyperglycemia. Oh, and by the way, here's some ketones on top, releasing those acidic ketones into the blood leading to acidosis.
So regarding some assessment findings of DKA, patients are going to have fruity breath. That's a hallmark sign of patients who have DKA.
Ketones because of that glycogenolysis, right? Dehydration can also occur, right? Also altered levels of consciousness, right? Our pH is low, less than 7. We can have altered levels of consciousness. We're also going to see, again, hyperglycemia, typically a capillary blood glucose greater than We're also going to be doing, regarding our assessment, Q1 hour glucose checks, as well as frequent neuro checks related to that altered levels of consciousness.
And we're also going to be checking Q2 hour BMPs. We're basically going to be looking at the amount of bicarbonate that their body is producing, wanting to make sure as we treat and correct their acidosis, we're wanting to make sure that their bicarbonate levels are getting back to a normal range, as well as, again, you'll remember from our ABGs video, bicarbonate is released to neutralize excessive acids and to restore a more normal blood pH level.
So how are we going to treat the patient in DKA? The first thing is we're definitely going to use regular IV insulin. Again, we are insulin deficient in a patient who has diabetes, first of all, much less than one in DKA.
On physical examination, signs of dehydration are often present, including dry mucus membranes, decreased skin turgor, tachycardia and hypotension.
In addition the smell of acetone on the breath and deep and laboured breathing Kussmaul breathing may be observed, particularly in patients with severe acidosis. This change in breathing is an attempt by the body to correct the metabolic acidosis and compensatory respiratory alkalosis Yehia et al, ; Umpierrez et al, Mental state can vary from full alertness to profound lethargy Umpierrez et al, Although DKA can be suspected on clinical observations, confirmation of the diagnosis is based on laboratory findings.
The laboratory investigation in DKA includes measurement of:. Further investigations may be carried out to identify potential infection or myocardial infarction as precipitating factors for DKA; these tests may include complete blood count, blood cultures, cardiac enzymes and ECG Kitabchi et al, Clinical presentation and laboratory investigations usually provide the information needed to diagnose DKA.
It is important to remember that not all patients who present with ketoacidosis have DKA Umpierrez et al, so when diagnosing DKA, other causes of ketosis should be considered, including starvation ketosis and alcohol ketoacidosis Yehia et al, ; Umpierrez et al, Other differential diagnoses include lactic acidosis, renal failure and drug intoxication Yehia et al, Box 1 outlines the JBDS criteria for diagnosing DKA.
DKA is a medical emergency and should be managed promptly JBDS, It is important to assess for severity to determine the clinical setting in which the patient is to be managed; criteria are outlined in Box 2. Patients exhibiting one or more of these signs should be assessed by a consultant physician and considered for referral to a high dependency unit:.
The management of patients presenting with DKA includes a full clinical assessment, while regular monitoring of vital signs and consciousness levels using the Glasgow Coma Scale is essential JBDS, Key areas in the management of DKA include:. Fluid replacement is one of the most important initial therapeutic interventions in the management of DKA.
Patients are usually dehydrated and correcting this deficit will result in significant metabolic improvement Kitabchi et al, The aims of fluid resuscitation are to:. Other causes such as heart failure, sepsis and factors such as age, sex and medication history should also be taken into consideration JBDS, Normal saline 0.
Rapid fluid replacement is usually required in the first few hours of treatment; most patients require between ml and 1L to be given rapidly JBDS, Special attention must be paid to fluid balance in patients at high risk of complications - these include older people, pregnant women, children and young people years , and those with heart and kidney failure JBDS, The aim of insulin therapy in DKA management is to suppress ketogenesis, reduce blood glucose and correct electrolyte imbalance.
Insulin therapy increases peripheral glucose use and decreases hepatic glucose production, thereby lowering blood glucose concentration. It inhibits the release of free fatty acids from adipose tissues and decreases ketogenesis Umpierrez et al, A continuous fixed-rate intravenous insulin infusion FRIII of 0.
The recommendation for preparation of insulin infusion is 50 units of human soluble insulin made up with 50ml normal saline 0. FRIII should continue until DKA is resolved. The JBDS recommends that background insulin should be continued along with the IV insulin infusion to reduce the risk of rebound hyperglycaemia when the IV insulin infusion is discontinued.
If background insulin is discontinued, a subcutaneous dose must be given before the IV insulin infusion is discontinued JBDS, The conversion to the subcutaneous insulin regimen should be planned around a mealtime; subcutaneous short-acting insulin should be given at the meal and then IV insulin discontinued one hour later JBDS, Blood glucose, ketones, electrolytes, including bicarbonate, and venous pH, should be monitored closely at or near the bedside.
Maintaining normal serum potassium and prevention of hypoglycaemia are important in the management of DKA as hypokalaemia low potassium level and hyperkalaemia high potassium level are both life-threatening conditions and common complications.
Prevention of hypoglycaemia is vital, so bedside blood glucose monitoring should be performed every hours JBDS, It is sometimes necessary to give dextrose infusions to stabilise blood glucose levels; this should be given concurrently with the sodium chloride infusions used to correct circulatory volume JBDS, To avoid complications related to rapid infusion it is important to monitor fluid balance and electrolytes closely.
Regular assessment for complications such as cerebral oedema and fluid overload is vital JBDS, The JBDS stipulates that the diabetes specialist team must be involved in the management of every patient admitted with DKA, and referral should be made as soon as possible during the acute phase.
Team members play an important role in assessing the precipitating cause of DKA, acute management, discharge planning, education and follow-up care including psychological support JBDS, The best-practice tariffs stipulate that people admitted with DKA must be referred to the diabetes team and be seen by a member of the team within one working day of admission Price et al,
Asesssment Care NursingEndocrineMed SurgPathophysiology. I assessnent have a Resveratrol and muscle recovery DKA STUDY GUIDE for you. And this leads Wind power generation unrsing ketones Strength and conditioning produced, which can lead to acidosis. Step 4: Ketones are produced because of that fat breakdown. And ketones are ACIDS! Step 5: Metabolic acidosis occurs because of all the acid build up in the blood. There are 3 main nursing interventions for DKA: fluids, insulin, and of course, continuing to assess your patient!
die Auswahl bei Ihnen kompliziert