DKA is defined as blood glucose > 250 mg/dL (although blood glucose levels can also be normal on some occasions), blood pH < 7.3, serum bicarbonate < 18 mEq/L, and the presence of elevated anion gap (AG) metabolic acidosis [6]. However, patients with DKALK present with blood pH > 7.4 and bicarbonate > 18 mEq/L [5, 6]. This limits their utility as diagnostic parameters and might mask or significantly delay diagnosis while other differentials of raised AG are investigated. DKA is a potentially deleterious complication of diabetes, and timely treatment relies on prompt recognition, hence novel assays like serum beta-hydroxybutyric acid (β-OHB), the major ketone body, makes it easier to use serum ketone measurement as an independent parameter for detecting ketoacidosis [2]. This facilitates speedy intravenous fluid therapy and electrolyte replacement which unmasks the underlying acidosis [6].

One of the defining features of the condition is profuse and or intractable vomiting [12, 13]. The patient may also have a history of self-medication with absorbable alkalis [14, 15]. Other symptoms and signs are in keeping with those of traditional DKA.

DKA usually manifests with acidaemia, however, it may occur as an alkalaemia in strange presentation with diuretics, intractable vomiting, and hyperaldosteronism [6].

Although signs of DKA (acidosis or alkalosis) might appear for several days prior to the development of ketoalkalosis or ketoacidosis, the condition often manifests itself within less than 24 hours. The history of the hyperglycaemic hyperosmolar state (HHS) spans several days to weeks. In addition, persons living with type 1 diabetics who are younger and slimmer tend to experience DKA, and persons living with type 2 diabetes who are older and obese are more likely to experience HHS [18]. Physical manifestations include Kussmaul breathing, elevated respiratory rate, fruity breath from acetone in diabetic keto-alkalosis and ketoacidosis, and indications of dehydration accompanying hypotension. Though fairly common in HHS, confusion is an uncommon manifestation of DKA. It is important to look into possible explanations as in HHS high serum osmolality (> 340 mOsm/kg) correlates better with confusion than blood glucose does [18]. A substantial proportion of patients with DKA also exhibit hyperosmolality and are classified under the combined condition known as DKA-HHS [19].

Another diabetic emergency is euglycemic diabetic ketoacidosis (EDKA). EDKA, is a tetrad comprising metabolic acidosis, increased AG, ketonemia or ketonuria, and normal blood glucose levels (< 200 mg/dL) [14]. Triggered by states like fasting, this condition presents a significant diagnostic challenge due to the euglycemic state concealing the presence of underlying DKA. The normal blood glucose levels can be misleading, masking the critical metabolic disturbances characteristic of DKA and thereby complicating timely diagnosis and appropriate intervention [14].

DKALK is a severe and potentially life-threatening complication of DM, characterized by hyperglycemia, ketosis, and metabolic alkalosis [6, 18]. Timely and accurate diagnosis is crucial for effective management and prevention of complications. Thus, we foray into the diagnostic strategies for DKA, focusing on laboratory tests and imaging techniques.

There is universal agreement that the most important initial therapeutic intervention in keto-alkalosis, like in ketoacidosis, is appropriate fluid replacement followed by insulin administration [24].

The main aims for fluid replacement are as follows [24]:

1.

Restoration of volume loss.

As it stands, the bulk of the available literature regarding fluid therapy is based on consensus guidelines and expert opinions [25]. Normal saline is recommended as the initial IV fluid replacement. Initial IV fluid replacement starts with 0.9% sodium chloride at a rate of 15–20 mL/kg (about 1–1.5 L) over one hour [25, 26]. Thereafter, the rate and type of fluids are determined by assessment of the stability of the clinical state [26].

DKALK has courted interest in current literature as a rare manifestation of diabetic emergencies, characterized by metabolic alkalosis rather than the typical acidosis seen in DKA [6]. Notable case studies have highlighted the clinical significance of this condition, often occurring in patients with complicating factors such as severe vomiting, alcohol abuse, or concurrent diuretic therapy [14].

The purpose of this literature review is to bring to awareness and remembrance the incidences of DKALK and the treatment approach employed in each circumstance.

One notable case demonstrated the diagnostic challenge posed by DKA, where a patient presented with severe vomiting and metabolic alkalosis, initially misdiagnosed as gastrointestinal illness [15]. Another case study underscored the importance of recognizing DKA in patients with unexplained metabolic alkalosis, leading to timely intervention and improved outcomes [16].

Table 2 summarises some notable reported case studies of DKA.

These meld of case reports and studies emphasize the need for heightened clinical suspicion and a comprehensive understanding of DKA as a potential “dark horse” among diabetic emergencies. Furthermore, they highlight the importance of tailored management strategies addressing both the underlying precipitating factors and the metabolic derangements unique to DKA. Continued research efforts are enjoined and warranted to refine diagnostic criteria, optimize therapeutic approaches, and enhance early recognition of DKA, ultimately improving patient outcomes in this challenging clinical scenario.

The implications of DKALK in clinical practice demand attention and are significant, emphasizing the need for heightened awareness and tailored management strategies. Recognition of DKALK as a distinct entity from DKA is crucial, as it presents with metabolic alkalosis rather than acidosis [2, 6]. Clinicians must maintain a high index of suspicion, particularly in patients with atypical presentations or complicating factors such as severe vomiting, alcohol abuse, or diuretic use. Prompt diagnosis and appropriate management are essential to prevent potentially life-threatening complications [6]. Furthermore, healthcare providers should ensure comprehensive evaluation and treatment addressing both the underlying precipitating factors and the metabolic abnormalities unique to DKA. Continued research efforts are necessary to refine diagnostic criteria and therapeutic approaches, ultimately optimizing clinical outcomes for affected individuals [14].

Risk assessment of DKALK involves recognizing predisposing factors such as severe vomiting, alcohol abuse, or concomitant diuretic use, which can precipitate this condition [6]. Additionally, patients with poorly controlled diabetes or a history of insulin non-compliance are at increased risk [7]. Clinicians should maintain a high index of suspicion in these individuals and consider DKALK in the differential diagnosis of diabetic emergencies. Timely recognition and intervention can mitigate the risk of severe complications associated with DKALK.

Huggins et al. [9] proposed a revision of the diagnostic criteria for DKALK to identify cases, facilitate prompt management and reduce misdiagnosis [9, 13]. The proposed diagnostic criteria (an extension of the existing accepted criteria) posits that when the elevated DR is above 1.2 or when the bicarbonate is variably elevated, the diagnosis is DKALK until proven otherwise. The DR is a ratio between the rise in the AG (> 12) and the drop in bicarbonate (< 18 mEq/dL) [9].