Dr Luke Phillips
Peer review: Dr David McCreary
Welcome to Fast Fridays – a case-based, rapid review of a topic. The cases have been adapted from real patients but have been changed for anonymity and to emphasise key learning points.
An 84-year-old presents with a 4-day history of cough, shortness of breath and some fevers/lethargy. Family report that they have had decreased oral intake throughout that time and have had polyuria. They have a history of Type 2 DM (insulin-requiring) and their BSL is reading “high”.
Based on the above, what do you think is happening?
I need to look for other precipitants of a HHS such as a myocardial infarction, surgical/GI issue that leads to excessive vomiting, evidence of stroke or intracranial pathology, any recent steroid use or compliance/changes with medications.
I wish it was still called HONK, but what is HHS?
It differs from DKA due to its insidious onset and its pathophysiology is caused by a combination of reduced ability to utilise glucose and a disease state causing elevated counter-regulatory hormones (aggh – primary exams 🤯) leading to gluconeogenesis and glycogenolysis. The result is hyperglycaemia and an osmotic diuresis.
A formal glucose (it came with a bowtie 🤵♂️) is 40mmol/L and blood ketones are 2 mmol/L. Your venous blood gas is outlined below.
Describe and interpret the VBG findings
- There is a primary mild-moderate metabolic acidosis
- Expected CO2 is 39.5 (1.5xHCO3 +8) while our CO2 is 48 therefore there is inadequate compensation and a concomitant respiratory acidosis (this may be related to the fact it is a venous gas).
- Given there is a metabolic acidosis I would calculate the anion gap ((Na+ + K+) – (HCO3– + Cl–) which in this case is 18 and therefore high – I would have suspicion for some renal impairment, ketones or any cause of poor perfusion (sepsis/MI) based on this and will go looking for it.
Further useful calculation would be:
- Osmolality (2xNA + Gluc + U)r): Even without the urea it is high at 308 mOsm/kg
- Corrected Sodium for glucose (Na + (Gluc-5)/3) = 146mmol/L
What are your management priorities?
This process has happened over days, so you don’t want to correct everything too quickly. The principles of managing HHS are outlined below.
- Identify and Reverse the Underlying Precipitant
- Replace Fluid Deficits:
- Initial resuscitation may be needed to restore the circulating volume with 0.5-1L Normal Saline boluses.
- Then gentle rehydration to restore the deficits over the coming 24-48hrs. Rapid correction of this deficit can lead to osmolar shifts and cerebral oedema. Our hospital guidelines recommend normal saline for this.
- 45% sodium chloride can be considered if the osmolality is not declining despite a positive fluid balance and the fall in glucose at a rate of 4-6mmol/L per hour is not being achieved.
- Electrolyte Monitoring and Replacement:
- Aim to lower osmolality by 3-8mOsm/kg per hour
- Sodium should not be lowered more than 10mmol in a 24hr period
- Commence potassium replacement early – Aim for K+ > 4mmol/L
- Insulin Therapy:
- Commence an insulin infusion at 1-3 units/hr as per your local guidelines.
- Insulin should only be started after fluid hydration underway, and the serum potassium is > 3.5mmol/L
- Consider starting earlier if ketones > 1mmol/L
- Commence on 5% dextrose when BG < 15mmol/L
- Ongoing Monitoring: Should be stabilised and monitored in a high dependency area with cardiac monitoring. The patient needs hourly BSL and venous blood gas for the first 6 hours then stretch the time frame of these depending on the patient’s condition. Close monitoring of urine output is also important to measure ongoing losses. ICU may be needed for patients with severe HHS, challenging to manage co-morbidities such as cardiac or renal failure or if they are frailer.
- Thromboprophylaxis: Similar to your DKA patients, HHS patients are at high risk for developing venous thromboembolic events.
Our patient was identified as having a missed anterior myocardial infarct with evidence of an established infarct on their ECG and a high-sensitivity troponin of 12000. A chest x-ray revealed evidence of pulmonary oedema, and this was confirmed with bedside ultrasound where there was widespread anterior B-lines and small effusions and a septal akinesis on echo.
The patient was started on the above therapy and transferred to ICU for ongoing care given challenges with fluid management. During their inpatient stay they had an angiogram which confirmed mid LAD lesion, and this was stented, and they were eventually transferred to a rehab facility for cardiac rehab.
References and Further Reading:
Life in the Fast Lane: https://litfl.com/hyperosmolar-hyperglycemic-state/
Emergency Medicine Cases: Ep 147 HHS Recognition and ED management
Alfred HHS Clinical Guidelines (available on Alfred Intranet)
Dr Luke Phillips is an Emergency Physician at Alfred Health in Melbourne and currently the Co-Director of Emergency Medicine Training. He is a passionate educator and has been fortunate enough to be able to combine this with his love of emergency ultrasound.
Luke has a special interest in the use of focused ultrasound for critically unwell patients, in trauma management and in the use of ultrasound to guide procedures and improve patient safety in the ED. He is currently the Co-Chair of the Emergency Medicine Ultrasound Group (EMUGS.org) Board of Directors and holds a number of CCPU units through ASUM.
Luke is also involved in the department’s international education program and has developed a Certificate of Emergency Medicine which is currently being run in both Germany and India. He also has interests in human factors, debriefing (particularly after clinical events), and simulation.
His Twitter handle is @lukemphillips.