When patients arrive in the ICU, as soon as they are settled, an AP portable chest x-ray (CXR) is ordered. That x-ray will look different from one done in the radiology department, as the patient is likely semi-recumbent, may be in expiration and the projection is different than from an CXR taken from the back.
The lung has 5 lobes – three on the right and two on the left (the left lung is smaller to accommodate the heart). Each one of these lobes is connected to the trachea by one major airway, that may become plugged off, resulting in atelectasis or collapse of the lobe. As we often need to remove mucus plugs or other material causing these obstructions, it is imperative that you are able to identify the particular lobe that has collapsed. I sequentially go through each lobe of the lungs.
To identify a collapsed lung lobe I suggest that you follow the “Ds” listed in the image below.
In addition, radiologists often report lung units as being “consolidated.” This is a catch all phrase that identifies the presence of liquid or semisolid material in airspaces – infectious exudate, blood, mucus, water-fluid, gastric contents etc. You should be able, with you anatomical knowledge, to identify which lung lobe is affected, in particular if you are planning on performing a broncho-alveolar lavage. @ccmtutorials
One of the most intimidating things about entering the ICU for the first time is the “life support machine” – the mechanical ventilator. Although I have posted an extensive series of tutorials on Mechanical Ventilation, covering most of the modes, oxygen therapy and applied respiratory physiology, I have attempted, in this tutorial, to distill everything to the “least you have to know” in 40 minutes. Keep in mind that modern machines look more like iPhones, and are far easier to use than the devices I grew up with that looked to me, on day 1, like something in the cartoon below.
I start with a discussion about the difference between normal breathing, CPAP and Positive Pressure Ventilation (PPV). PEEP is, effectively, CPAP during PPV. I then go on to discuss pressure limited modes of ventilation; worldwide this are the most widely used modes in ICU. I limit my discussion to Pressure Assist Control, Volume Guaranteed Pressure Control (VG_PC) and Pressure Support Ventilation (PSV). VG-PC is a popular and flexible option as an ICU’s default mode. However, as it is a pressure controlled mode, there is significant variability in tidal volume and airway pressure from minute to minute.
Several important rules are emphasized: the tidal volume should, in general be lower than 6ml/kg of ideal body weight, the plateau pressure lower than 30cmH2O and the driving pressure lower than 15cmH2O. I introduce the Spontaneous Breathing Index (SBI = RR/TV in L). The magic number is 100. We use the SBI to determine the success of weaning on PSV.
Volume Controlled Ventilation is the predominant mode use in the Operating Rooms (Theatres), and Volume Assist Control is a popular mode in North America. In ICU you must set a peak inspiratory flow and be aware that this may be insufficient during assisted breaths and lead to dys-synchrony. Volume Control is often used in ARDS to “lock in” the Tidal Volume (TV) but the operator must be aware that the TV that matters is not what is dialed up on the ventilator, but what the patient exhales.
I go on to discuss how to assess the patient on invasive mechanical ventilation, by looking at whether they are breathing spontaneously, in which case we determine whether they are suitable for a Pressure Support wean or not, or whether or not there is a problem with oxygenation (increase FiO2, PEEP, Mean Airway Pressure and seriously consider Prone Positioning) or Ventilation (increase Respiratory Rate, Tidal Volume or both, reduce PEEP).
The final part of the tutorial looks at Non Invasive Ventilation (NIV), and I explain how, in general we only use 2 modes on standalone devices – CPAP and Spontaneous Timed (S/T). The latter is similar to PSV with a backup rate, but I point out that instead of PEEP+PS the breath is EPAP + IPAP and IPAP is not built upon IPAP, as is the case with PSV. If one is delivering NIV on an ICU ventilator, then “leak” adjustment or “leak sync” should be used.
This tutorial looks at the assessment of PaCO2 on the blood gas and how it interfaces with the pH and the Bicarbonate (HCO3-). The control of PaCO2 is a major physiological mechanism for maintaining homeostasis. CO2 production by the body must be balanced by CO2 elimination. PaCO2 rises when there is hypoventilation, this results in a fall in pH and an rise in HCO3 and this is called “Acute Respiratory Acidosis.” If the patient hyperventilates, the PaCO2 and the HCO3 fall and the pH rises: this is “Acute Respiratory Alkalosis.” When there is chronic CO2 retention, the body adapts by wasting Chloride in the urine, the pH normalizes and the HCO3 rises substantially.
Any patient who is intubated, or who has a laryngeal mask in situ, must undergo end tidal (end of exhalation) CO2 monitoring. The capnography waveform is worth evaluating, particularly if airway obstruction or increased resistance is suspected.
Included in this tutorial are various rules of thumb that you can use to determine the Respiratory Acid Base Status of the Patient – including the “Rule of 40.”
The majority of patient who are admitted to ICU require targeted oxygen therapy during the course of their stay. This tutorial looks at how we assess oxygenation.
The easiest method for assessing oxygenation is to use the PaO2/FiO2 ratio (PFR) as a method of aligning the inspired oxygen tension (the therapy) to the PaO2 (the goal and the response). The PF ratio has been a key component of the diagnostic criteria for ARDS for decades. The PaO2 is measured by performing a blood gas. It represents dissolved oxygen in plasma rather than the oxygen content of blood that is determined by the oxyghemoglobin concentration and saturation (SaO2). The SaO2 can be helpfully estimated using non invasive pulse oximetry (SpO2).
Oxygen is taken up from the lungs continuously and carbon dioxide is excreted. Breathing is cyclical. Most gas exchange occurs during expiration, as inspiration only occupies 10 seconds or so per minute. The lungs hang down in the chest and hang out at a resting volume known as Functional Residual Capacity (FRC) at end expiration. Anything that reduces FRC, reduces the surface area for gas exchange and results in stale gas in or atelectasis of the alveoli. The consequence is ventilation perfusion mismatch and hypoxemia.
The initial treatment for hypoxemia is oxygen therapy delivered through nasal cannula. If that fails, or the patient is distressed, then high flow nasal oxygen (HFNO) is delivered. This improves oxygenation and reduces the work of breathing. If high flow fails, CPAP is delivered. CPAP applies positive pressure throughout the respiratory cycle, preventing phasic atelectasis and redistributing gas withing the lung. FRC is restored. If the patient fails HFNO, then they are intubated and ventilated.
Oxygen is assessed using FiO2, oxygen flow rate, PEEP or CPAP and mean airway pressure.
I am now going to move on, in the Introduction to Critical Care course, to a systems based assessment of the patient where you are expected to compile measurements and observations from the clinical information system, radiologic system and monitors to construct an overview of the patient’s status. This is the crux of intensive care medicine and it is not easy. I am going to visit each system sequentially, and some systems will have multiple tutorials. By the end of this process, you will have compiled all of the data, assessed and processed it, and be ready for the big presentation.
The first tutorial in this part is an overview of patient assessment. It is relatively short but essential.
The Second tutorial in this sequence is on at neurological assessment in the ICU. It contains a discussion about the Glasgow Coma Scale, The Richmond Agitation Sedation Scale and CAM-ICU. I also cover the assessment of suffering (PAID) in critical care.
You will need to assess the patients neurologic status, whether or not they appear to be suffering and what interventions, both environmental and pharmacological, that you are administering to help them.
The Critically Ill Patient should receive a systematic head to toe front to back clinical examination each day. Before you start, stand at the end of the bed and take in the scenery. An experienced ICU doctor will acquire an enormous amount of information about a patient by eyeballing the monitor, looking at the patient’s habitus, the machines, the other attached devices, infusion pumps etc.
Then INTRODUCE yourself and explain to the patient, irrespective of level of consciousness, that you are going to examine them, if that’s ok.
Does the patient have an endotracheal tube, nasogastric tube (is it on free drainage?), enteral feeding tube (yellow) or orogastric tube).
Follow the pattern of Inspection, Palpation, Percussion and Auscultation.
Start with the head and evaluate its shape and color. Then move on to the eyes, nose, lips, mouth (inside and outside) and then on to the side of the head and ears.
Move on to the neck – observe for masses, scars and lines (what type of line). Palpate the neck paying particular attention to the trachea (you may want to do a tracheostomy down the line). Feel for crepitus in the supraclavicular area.
Move on to the chest – inspect – look for recent surgical wounds and scars, chest or mediastinal drains, pacemaker wires etc. Observe the breathing pattern – is it symmetrical? Palpate the cardiac apex and the left sternal border. Auscultate for cardiac murmurs, carotid bruits and for breath sounds, looking for loss of air entry, crackles or bronchial breathing.
Move on from the chest to the arms – are they symmetrical? Is the patient moving both arms? Any redness? What color are the fingers – any mottling? Are the fingertips necrotic? Palpate the arms and hands and feel the temperature – hot or cold? Feel the brachial and radial pulses.
Move on to the abdomen: is it scaphoid or globular? If globular consider the 5 Fs: fat, fluid, flatus, feces, fetus. Are there any scars, wounds or drains? Palpate, percuss and auscultate the abdomen.
Move on to the legs. Are they moving? Are they equal in size? Are the quadriceps wasted? Is there mottling or ischemic changes? Is the patient wearing compression stockings (TED) and or sequential compression devices (SCD)? Palpate the legs, feel the pulses and then look at the ankles (pitting edema) and heels (pressure sores).
Assess the skin – are there any rashes? Are they localized or generalized? If generalized is the rash macular, maculo-papular, vesicular (one side consider herpes zoster) or – ominously purpuric. A generalized purpuric rash is either meningococcemia or thrombotic thrombocytopenia purpura until otherwise proven (both disorders are immediately life threatening).
Roll the patient on their side and look at the back – in particular look at the pressure areas and at any pain catheters and their sites (epidural). Look for the presence of a rectal tube and bowel management system.
When you have completed examination, look at the devices around the bedside sequentially. Start with the main monitor and evaluate the ECG – rate (paced?), rhythm, shape (ST segment changes?). Then the pulse oximeter, arterial blood pressure – invasive and non invasive (correlating?), then the temperature and end tidal CO2 (and waveform).
Move on to the ventilator – if one is attached and note whether the patient is breathing spontaneously or not (why?), what mode (AC, SIMV, BiLevel, PSV), rate, tidal volume, fiO2, PEEP, PFR, plateau pressure, and dynamic compliance and resistance).
Is the patient receiving continuous kidney replacement therapy – note the mode (CVVHDF or SCUF), anticoagulation strategy (citrate or heparin), and fluid removal.
Look for intravenous and enteral feed and take note of the rate and the contents. Then move on to the infusions – iv fluids and electrolyte replacement, analgesics and sedatives, vasopressors, inotropes, insulin and corticosteroids.
Before leaving the bedside look around – did you miss anything and machines or drains or infusions? Then clean up any mess that you have made, restore the bedspace to the condition it was in and inform the nurse of any changes you made or any new observations.
This tutorial has been broken up into two videos to make them easier to navigate.
Before approaching an critically ill patient’s bedside you should know who the patient is and why they are in the ICU. The purpose of the history is to lay out the known facts about the patient. Usually the patient in the ICU is unable to give a clear and reliable history. You need to comb through the patient’s chart to locate this information. Dig deep! Events that may have happened months ago may have an impact on the patient today. Don’t forget, you are not the only professional that is treating the patient: ask the nurse – they are excellent historians as they give and receive a concise report at the beginning and end of each shift. It is also worth talking to the primary team, physiotherapist, pharmacist and dietician about the patient. Remember, you are one member of a team: the others may have more knowledge of the patient than you. Nevertheless you need to remain a little bit skeptical about the story that you have been given: make sure the facts match the narrative
In this tutorial I will introduce the 4 Ws of clinical history: Who is this patient? Why are they in hospital and ICU. 3. What is going on with the patient (PROBLEM LIST). 4. Where are we going (what are the physiologic goals and organ based plans?).
WHO? Who is this patient? How old are they? Where do they come from and what is their occupation? How long has this patient been in the ICU – is this a recent admission (the patient is acutely critically ill and likely still being resuscitated)? Has the patient been in the ICU for more than 7 days? In that case the patient may be slow to recover or chronically critically ill.
What type of patient are we dealing with? Surgical or Medical? Postoperative or Critically Ill?
There are three types of critically ill patients: 1. Medical patients with an acute medical syndrome that may have occurred in the setting of low physiologic reserve. These may be children or adults. 2. Surgical patients – who have had complex elective surgery (e.g. cardiac or neurosurgery), emergency surgery or trauma. The patient may have originated as a surgical patient but now has medical problems (e.g. hospital acquired pneumonia). 3. Obstetric patients who may be currently pregnant, recently pregnant and be in ICU as a consequence of pregnancy (pre-eclampsia, post partum hemorrhage) or co-incidental with pregnancy (trauma, bowel obstruction etc.).
WHY?
It is absolutely CRITICAL that you understand the dynamics around the patient’s ICU admission. The patient may have come directly from the emergency room or operating room to ICU, or may have been transferred from a ward or other hospital. In the latter case you will need to ensure that you know exactly what went on there. These are the questions that you must ask, up front about the patient.
Why was the patient admitted to hospital? Why was the patient admitted to ICU? What happened in between?
What was the patient’s admission problem (MAJOR ADMISSION PROBLEM)?
This is the patient’s presenting problem (although it may not be the patient’s main current problem). It is the symptoms and diagnosis that led the patient to come into the hospital originally – e.g. chest pain, shortness of breath, confusion. This may be clarified as “pneumonia” “septic shock” etc.
Between the patient arriving in the hospital and being admitted to ICU clinical episodes may have occurred – you need to know these. Was there a delay with the diagnosis? Was a wrong pathway chosen? Did the patient deteriorate or have a cardiac or respiratory arrest on the ward?
What was the patient’s indication for ICU ADMISSION
This is a remarkably limited list because patients are admitted to ICU for life sustaining therapy consequent of single or multi organ failure. Those injuries can be summarized as follows:
Neurological – Low GCS, Seizures
Cardiovascular – Hypotension, Arrhythmias, Blood Loss
Some patients, for example those with septic shock, may have multiple system problems: confusion, hypotension, hypoxemia, oliguria – AKI.
What complications followed?
Prolonged admission to intensive care is characterized by “second and third hits” – organ injuries such as hospital acquired pneumonia, line sepsis, myocardial ischemia, acute kidney injury, bed sores etc. It is important that you are aware of these problems even if they have now resolved, as complete recovery of organ function at this stage is unlikely, and those organs remain vulnerable (for example, it is important that you do not prescribe non steroidal anti inflammatory agents (NSAIDS) to a patient who has recently recovered from acute renal failure).
What is the patient’s age and baseline health status (BACKGROUND)?
What background medical problems does the patient have? We know that patients with major organ dysfunction (such COPD, pulmonary fibrosis, heart failure (EF<40%), chronic kidney disease, cirrhosis or chronic hepatitis, previous myocardial infarction or active ischemia, connective tissue disease, inflammatory bowel disease, cancer, cerebrovascular disease, carotid arterial disease) have diminished physiologic reserve, and have a worse prognosis when admitted to intensive care. The greatest determinant of outcome, however, is the patient’s age: young patients do better in intensive care than older ones. You also need to know what medications the patient was taking pre-admission: antihypertensives, statins, SGL2 inhibitors, GLP-1 receptor agonists etc. If the patient is taking anti-coagulants you need to know why? Pulmonary embolism, stroke, atrial fibrillation, arterial obstruction, heart valve etc. All of this is relevant.
WHAT?
What PROBLEMS are keeping this patient in intensive care (CURRENT PROBLEMS)?
The patient may remain in ICU for a problem wholly unrelated to the original presenting complaint – failure to liberate from mechanical ventilation, failure to emerge from sedation etc). This is the patient’s main current problem, and it needs to be addressed. In addition, it is important to enumerate the other problems, even if they are apparently trivial.
If you don’t have a precise diagnosis don’t invent one – just list the problems, these can be padded out later
So a patient may be admitted with Hypoxic Respiratory Failure That might evolve to Ventilator Dependent Respiratory Failure That Becomes Acute Respiratory Distress Syndrome Clarified as Community Acquired Pneumonia, secondary to culture positive Staphylococcus Aureus
To identify the problems you need to evaluate the patient’s organ systems in an organized, precise and systematic way. The way I go through the systems is as follows:
NEUROSYSTEM
•The patient has a “Low GCS secondary to….” traumatic brain injury (specify), stroke, encephalopathy, encephalitis, meningitis, cause uncertain etc.
•The patient has “Severe Delirium with a RASS score of…..being treated with…..
•The patient is in “Status Epilepticus being treated with…..with a know or no known history of Epilepsy”
•The patient has “Guillain Barre Syndrome, requiring mechanical ventilation being treated with plasma exchange”
RESPIRATORY SYSTEMPROBLEMS
Problems with the respiratory system are usually 1. problems with the lung parenchyma (gas exchange) or 2. problems with the airway (particularly airway obstruction)
Parenchymal Problems
Acute Hypoxic (AHRF) or Hypercarbic Respiratory Failure
Although rhythm disturbances causing hypotension are technically “cardiogenic shock” nobody really uses that term, generally we describe the problem
•Complete Heart Block requiring external pacing
•Fast Atrial Fibrillation requiring an amiodarone infusion
•Runs of Non Sustained Ventricular Tachycardia requiring……
KIDNEY PROBLEMS
•The patient has “Acute Kidney Injury secondary to (sepsis or rhabdomyolysis or prolonged hypotension) requiring Continuous Kidney Replacement Therapy”
•You might also qualify this with “on a background of CKD”
•“Dialysis Dependent AKI – he receives intermittent hemodialysis for 3 hours each day”
•“AKI no longer requiring Kidney Replacement Therapy”
The patient may have been admitted with a hematology issue e.g. thrombotic thrombocytopenia purpura (TTP) or a complication of chemotherapy or bone marrow transplantation Otherwise
•Anemia, Polycytemia, Thrombocytopenia
INFECTIOUS PROBLEMS
The infection may be the primary problem or it may be secondary
•Wound contaminated with VRE or Pseudomonas
•Patient may have acquired MRSA
•Patient may be isolated due to CPE
RESOLVED PROBLEMS
•If the patient was admitted with sepsis – source control may have resolved the problem
•An underlying cardiac problem may have been fixed by a stent
•An obstructed bowel or leaking aneurysm may have been surgically repaired.
•Acute kidney injury may have resolved
•Is anything ever fully resolved?
WHERE?
We can’t determine where we are going if we don’t know where we are now! From the outset, the physiological parameters under your control must be targeted: level of sedation, heart rate, Blood pressure, PaO2, PaCO2, pH, urinary output, enteral feeding, fluid balance, mobilization etc.
What physiologic targets have we set for this patient?
•Neurological – RASS score (or GCS) target with sedation
You don’t need notes to present a quick history, summary, problem list and goals of therapy. This should be drawn from memory as often the history is presented several times a day at handovers, rounds etc. Keep the narrative succinct – don’t stray off track – we are interested in the FACTS the FACTS and nothing but the FACTS.
Follow the system in the image below:
This Mr Eddie Chambers he is a 73 year old retired farmer from Mayo He is a medical patient He has been in the ICU for 4 Days………having originally been admitted with acute hypercarbic respiratory failure secondary to pneumoni He was admitted to ICU for intubation and mechanical ventilation He subsequently developed septic shock and acute kidney injury, requiring pressors and RRT He has a background history of hypertension treated with calcium channel blockers. His current problems are: ventilator dependent respiratory failure, pressor dependent septic shock and dialysis dependent acute kidney injury He is also malnourished, due to gastroparesis, hypoalbuminemic, anemic and has a hyperchloremic metabolic acidosis and stress hyperglycemia He also has an early sacral pressure sore
Our goals are to: Sedate to a RASS score of minus 2 Reduce the ventilator settings Keep the PaO2 above 8kPa (60mmHg) Keep the PaCO2 between 5.3 and 6kPa (40-45mmHg) A MAP of 70mmHg Fluid balance of -1000ml today on Kidney Replacement Therapy We are starting TPN today, and targeting a Blood glucose below 10mmol/L (180mg/dl) Sit him out in a chair today
REVIEW
This Tutorial Looked at Getting a History in the ICU. It is not easy because the patient is usually not able to communicate effectively. Significant detective work may be required.
Who – who the patient is
Why – the patient came to hospital and why they needed to be admitted to ICU
What is currently wrong with the patient (Problems)
Since the 1920s it has been known that administration of chloride rich intravenous fluids, characterized by a reduced Sodium to Chloride strong ion difference (SID), causes a progressive metabolic acidosis. This iatrogenic hyperchloremic acidosis was particularly problematic in the era before lactate and ketone measurement was widely available, prolonging critical care stay and resulting in, often, unnecessary tests and therapies. During the 2000s a body of literature emerged supporting the hypothesis that hyperchloremia, defined as a plasma chloride of greater than 110mmol/l may be harmful. In a series of retrospective analyses, hyperchloremia was associated with increased mortality across a spectrum of disorders, including surgery and critical illness. Hyperchloremia was also associated with increased risk of kidney injury and the requirement for renal replacement therapy. There was also some data that hyperchloremia may be associated with reduced splanchnic blood flow.
A series of papers that looked at isotonic saline solution (ISS – 0.9% NaCl ), often referred to as “normal” saline, versus Plasmalyte 148 (PL) in Diabetic Ketoacidosis (DKA), demonstrated that ISS was associated with prolonged duration of stay in critical care, usually associated with persistent metabolic (hyperchloremic) acidosis. No studies to date have demonstrated superiority of ISS to PL Four major clinical trials – SALT ED, SMART, BaSics and PLUS– were conducted to compare outcomes of acute and critically ill patients randomized to either balanced salt solutions (sodium lactate products – Hartmann’s, Lactated Ringers or PL) or ISS. The first 2 studies demonstrated that ISS was associated with renal dysfunction and worse outcomes with sepsis. The BaSics and PLUS trials, in their initial reporting, showed no outcome differences. However, these trials were “catch” all ICU studies, including perioperative patients, patients pre-resuscitated with ISS, and, overall very little fluid was administered. The studies were grossly underpowered to detect outcome differences. However, subsequent systematic reviews and meta-analyses that included these data, and subgroup analyses of high risk patients, determined that fluid resuscitation with ISS was associated with worse 30 mortality, particularly in sepsis, and worse renal outcomes.
It is my view that, based on decades of research and experience, “normal” Saline (ISS) should not be used as a first line agent for fluid resuscitation in critical illness. I believe that the current international guidelines for the management of DKA are flawed in that they continue to recommend the administration of an agent that may well be toxic to patients, particularly when alternatives are easily available. Watch the video and make up your own mind.
Hyperchloremic Acidosis is a common problem. It is usually an iatrogenic problem. Unfortunately, the majority of doctors who cause a patient to have Hyperchloremic Acidosis (HCA) are either unaware of the problem or ambivalent to it. For the most part, HCA is caused by the intravenous administration of isotonic saline solution (NS – “normal saline – NaCl 0.9%). This problem has been known about for more than 100 years and led Alexis Hartmann, a pediatrician from St Louis, to construct a balanced intravenous fluids, that he called “Lactated Ringers” solution. Ironically, in clinical practice, HCA is induced as part of the local hospital “protocol” for management of Diabetic Ketoacidosis. Inevitably, as the ketones fall, the Chloride rises, and the acidosis persists.
HCA is the only cause of “normal” anion gap metabolic acidosis and is almost always caused, . In the tutorial I explain that HCA is caused by a reduction in the Na-Cl strong ion difference (SID). The acidosis associated with NaCl 0.9% is more complex that merely a rise in plasma Chloride. Other serum electrolytes, Albumin and Hemoglobin are diluted – and this has an alkalinizing effect. Other resuscitation fluids have different impacts on acid base. Hyperchloremia is also a feature of Renal Tubular Acidosis (RTA), various other nephropathies, the administration of acetazolamide and other drugs, and following surgical transplantation of the ureters into the small bowel, If renal function is normal, and the Chloride level is lower than 125mmol/L, then the patient’s kidneys will resolve the problem over 36 to 48 hours. If the Chloride is very high, acidosis will persist, particularly in patients with poor renal function, and Sodium Bicarbonate infusions may be warranted.
This tutorial looks at an emerging problem in medicine – iatrogenically induced eugylcemic ketoacidosis, associated with the use of SGLT2 (sodium glucose cotransporter 2) inhibitor drugs, also known as Flozins.
There is a global pandemic of metabolic disease caused by escalating ingestion of carbohydrate rich ultra processed food. This results in central obesity, hepatic steatosis (fatty liver) and insulin resistance: together these findings are labelled the “Metabolic Syndrome” (MetS). MetS is associated with systemic inflammation and atherogenesis. In many cases it progresses to Type 2 Diabetes (T2D), the majority of treatments for which increase adiposity and escalate insulin resistance. SLGT2 inhibitors are a relatively new class of drug that work by increasing excretion of ingested glucose by blocking the Sodium-Glucose symporter channel in the proximal tubule of the nephron. The result is mild natiuresis and glycosuria. These agents have been proven effective in the management of T2D and are emerging as effective treatments for other diseases such as congestive cardiac failure and nephropathy. As the name of each of these medications involves the suffix -flozin – they are commonly termed “Flozin” drugs.
One of the major problem with the use of Flozins in the community is failure to discontinue the drug when fasting or not consuming calories. Glucose will continue to be wasted, often generated by gluconeogensis, suppressing insulin secretion, resulting in lipolysis and ketosis. As blood glucose is low there is insufficient insulin present to prevent ketoacidosis. This is one of the causes of euglycemic diabetic ketoacidosis (EDKA). EDKA is associated with both ketoacidosis and hyperchloremic acidosis.
The treatment of EDKA is dextrose (to restore the Kreb’s cycle and suppress ketosis) and insulin – to put some control on the metabolic system. The patient may require a couple of liters of resuscitation fluid – preferably sodium lactate solution (Hartmanns or LR). The ketosis resolves rapidly, but the acidosis resolves slowly because it is principally driven by hyperchloremia. Patients who are being treated with SGLT2 inhibitors that are scheduled for surgery should stop taking these drugs 3 days pre-op. If they are continued inadvertently or surgery is emergent, then a dextrose infusion should be considered and ketones checked routinely.
ORtoICU 