1. Introduction

With an estimated 13.3 million cases each year, acute kidney injury (AKI) become a problem for world health. In underdeveloped nations, there are 11.3 million cases every year. Globally, it results in 1.7 million deaths annually; 1.4 million of those deaths occur in low- and middle-income nations. AKI affects 15 to 20% of hospitalised individuals in wealthy nations, whereas it affects 25 to 30% of those in underdeveloped nations [1].

Data on the prevalence, causation, and prognosis of the condition are not entirely known. Acute diarrheal illness, malaria, leptospirosis, snakebites, insect stings, intravascular hemolysis brought on by septicemia, and chemical poisonings (copper sulphate, Vasmol, and pregnancy) are the most typical causes of AKI in India. They make up 40% of all Aki in India [2,3,4].

In the literature, the range of renal failure in the adult population and the variables indicating a bad outcome are not clearly characterised. Planning efforts to prevent AKI and give priority to scarce and expensive therapy modalities is made easier when risk factors and poor prognostic markers are identified in these patients, especially in developing nations.

Different regions of India have different etiologies, courses, and outcomes. According to [5], the volume depletion caused by gastrointestinal fluid loss (35.2%) was the primary etiological factor for acute renal failure (ARF) that was seen. Similar findings were made by Mahajan et al., [6], who reported that volume depletion was the most frequent cause of ARF, and by Jayakumar et al., who discovered that acute diarrheal illness was the most frequent medical cause of ARF [5,6].

India has a high prevalence of AKI following volume depletion from gastrointestinal fluid loss. Due to poor socioeconomic situations, limited access to care, a lack of awareness of personal cleanliness, crowding, and climatic factors that encourage the spread of infection, diarrheal illnesses are widespread in India. AKI following gastroenteritis is probably caused by a lack of medical facilities in rural areas and a delay in treating dehydration.

One of the main causes of AKI in the tropics is decreased intravascular volume in patients with viral gastroenteritis, bacillary dysentery, cholera, and food poisoning [7]. This study was carried out to investigate the clinical and biochemical correlation and outcome of AKI related to gastroenteritis because diarrhoea is one of the common causes of AKI in tropical regions.

Hence, an understanding of the disease's clinical spectrum is needed to devise methods to improve the outcome due to this problem.

2. Materials and Methods

This is a prospective observational study conducted on 50 patients with AKI due to Acute Gastroenteritis admitted to Narayana medical college & hospital, Nellore, Andhra Pradesh, from Novmeber 2021 to October 2022.

2.1. Inclusion Criteria

1. All patients with AKI due to Gastroenteritis
2. All patients of either sex and age above 18 years
3. The serum creatinine level must rise gradually over 48 hours to \(0.3 mg/dl (26.5 mmol/l)\), reach 1.5 times baseline in 7 days, or decline by 0.5 \(ml/kg/h\) for 6 hours.

2.2. Exclusion Criteria

1. AKI brought on by conditions other than gastroenteritis is not included.
2. Patients with acute gastroenteritis who also have chronic kidney disease (CKD).

The diagnosis of acute kidney injury was used when there was evidence of kidney injury in some clinical settings without any kidney disease history. The term acute kidney injury was used when there was a rise in Serum creatinine \(\geq44 \mu mol/L (\geq0.5mg/dL)\) and the history of decreased urine output of less than \(0.5ml/kg/hr\) for more than 6 hrs.

The criteria used for AKI in the study was RIFLE criteria (given by Acute Dialysis Quality Initiative Group 2004) and is as follows.

There are many causes of acute kidney injury, of which we used acute gastroenteritis in this study.

• Acute Gastroenteritis- History of Passage of abnormally liquid or unformed stools at an increased frequency stool weight \(>200 g/d < 2\) weeks in duration.

3. Diagnosis of Azotemia

Laboratory evaluation for azotemia includes Blood Urea Nitrogen BUN/Cr, urinary sodium (Na), urea, urine osmolality (Ur Osmo), urinalysis (UA).

3.1. BUN greater than 21 mg/dL

Significant findings for prerenal azotemia

• BUN: Cr ratio greater than 20:1
• Fractional excretion of sodium (FeNa) less than 1, fractional excretion of urea (FeUr) less than 35%
• Urine osmolality 500 \(mOsm/kg\)
• UA can show hyaline casts [5]

3.2. Diagnosis of ATI or acute tubular necrosis (ATN)

ATI was synonymous with acute tubular necrosis (ATN). However, frank tubular epithelial necrosis is only 1 histologic pattern observed in clinical ATI and may reflect particular etiologies and/or severity of injury. The diverse pathologic changes are often dynamic and may differ by the timing of kidney tissue procurement and etiology.

3.3. Data collection

The length of the gastroenteritis and the interval between the beginning of GE and the development of renal failure were noted. At the time of admission, the patient's level of hydration was noted. Daily tests and records were made for blood urea, serum creatinine, and electrolytes. Other laboratory tests were performed, including the complete blood count (CBC), the erythrocyte sedimentation rate (ESR), the human immunodeficiency virus (HIV), the blood glucose level, the total leukocyte count and differential count, the erythrocyte sedimentation rate, and the liver function test.

4. Statistics

Frequency and percentage were used to summarise categorical variables. Mean, SD, and Median were used to represent continuous variables. For all 2 X 2 tables, the chi-square test and Fisher's Exact test were used to determine the association between categorical independent and dependent variables. Small counts rendered the p-value of the Chi-Square test invalid. A p-value of 0.05 or lower indicates statistical significance in all two-sided tests of significance. Version 22.0 of the Statistical Package for the Social Sciences was used to analyse the data.

5. Results

There were 50 Patients with Acute Kidney Injury due to gastroenteritis were included in the study.

Table 1. Age group.

Age group	Number			Percentage
	Male	Female	Total
<24	4	1	5	10.0
25-34	8	2	10	20.0
35-44	5	3	8	16.0
45-54	2	4	6	12.0
55-64	6	4	10	20.0
>65	7	4	11	22.0
Total	32	18	50	100

They were between the ages of 20 and 70, with a mean age of 49.02 years. The maximum incidence was seen in the age group \(>65\) years, followed by 25 to 34 years & 55-64 years, respectively in Table 1.

Table 2. Mean Age of pre-renal ATN patients and in survivors vs non-survivors.

Category	Mean Age (Years)	P-value
Males	47.12 \(\pm\) 6.03	0.156(ns)
Females	52.38 \(\pm\) 5.21
Pre Renal Azothemia (29)	49.3 \(\pm\) 5.66	0.16(ns)
ATN (21)	48.6 \(\pm\) 7.40
Survivors	46.73 \(\pm\) 4.75	0.21(ns)
Non-Survivors	65 \(\pm\) 6.034

The mean age of the pre-renal group was 49.3 \(\pm\) 5.66 years, and in the ATN group, it was 48.6 \(\pm\) 7.40. The mean age in survivors was 46.73 \(\pm\) 4.75, and that of non-survivors was 65 \(\pm\) 6.034. Pre Renal Azotemia, which was the most common kind of renal failure in this study, was followed by Acute Tubular Necrosis, 42% in Table 2.

Table 3. Patients and dehydration levels and outcome.

Severity	No	Survivours	Non-survivors
Mild	17	17	0
Moderate	20	19	1
Severe	13	6	7
Fluid Overload	3	1	2
No dehydration	-	-	-

In Table 3, 20 (40%) of patients had moderate dehydration. 17 patients had mild dehydration, 13 patients had severe dehydration, andfluid Overload was observed in 3 patients. The majority of non-survivours belong to the group of moderate and severe dehydration.

Table 4. Time between the beginning of GE and the emergence of ARF.

Category	The interval between onset of GE and the development of ARF
Pre Renal	4\(\pm\)0.23
ATN	5.19 \(\pm\) 0.68
Survivors	3.71\(\pm\)0.40
Non-Survivors	5.75\(\pm\)0.88

The mean interval between the onset of GE and the development of ARF was 3.0 \(\pm\) 2.9 days. It was \(3.71 + 0.40\) days in survivors and \(5.75 + 0.88\) days in non-survivors. In the pre-renal group, it was \(4+0.23\), and ATN was \(5.19 + 0.68\) days in Table 4.

Table 5. Mean creatinine concentrations at baseline, peak, and discharge.

Creatinine (Mean)	Overall Patients (0n admission)	Pre-renal	ATN	Non-survivors
Baseline	3.03 \(\pm\) 0.37	2.70 \(\pm\) 0.29	3.48\(\pm\)0.77	4.7\(\pm\)1.25
Peak	4.73 \(\pm\) 0.48	4.13\(\pm\)0.59	5.56\(\pm\)0.66	7.36\(\pm\)0.52
At the time of Discharge	2.87 \(\pm\) 0.39	2.42\(\pm\)0.33	3.48\(\pm\)0.42	4.11\(\pm\)0.79

In Table 5, On admission, Baseline creatinine with a mean of \(3.032+0.37mg/dl\). It was \(2.70+0.29\) and 3.48\(\pm\)0.77 inpre-renal and ATN groups. Themean peakcreatinewas \(4.73+0.48mg/dl\). It was \(4.13 + 0.59\) in pre-renal and 5.56\(\pm\) 0.66 in ATNgroups, respectively. The Mean creatinine at the time of discharge 2.87 \(\pm\) 0.39 mg/dl. The mean peak creatinine was 2.42 \(\pm\) 0.33 in pre-renal & \(3.48+0.42\) in ATN groups (In survivors) and 4.11\(\pm\) 0.79 in non-survivors.

Table 6. Mean blood urea levels at time of discharge, baseline, and peak.

Blood Urea	Overall Patients (0n admission)	Pre-renal AKI	ATN	Non-survivors
Baseline	120.44\(\pm\)18.13	126.41 \(\pm\) 15.52	112.19\(\pm\)24.94	177.75+56.36
Peak	153.76\(\pm\)12.29	139.10 \(\pm\) 14.72	174 \(\pm\) 17.62	201.75+13.92
At the time of Discharge	86.28\(\pm\) 9.07	78.93+13.44	96.42+12.97	133+16.50

In Table 6, At admission, the urea levels ranged between 69 to 251 \(mg/dl\) with a mean of 120.44 \(\pm\) 18.13 \(mg/dl.\) The peak meanurea level was observed as 153.76 \(\pm\) 12.29 mg/dl. At the time of discharge, the urea levels ranged between 35 to 181, with a mean of 86.28 \(\pm\) 9.07mg/dl. The mean peak urea levels in survivors were175.0 \(\pm\) 65.5, and in non-survivors were 201.75 \(\pm\) 13.92 mg/dl.

6. Discussion

The glomerular filtration rate rapidly decreases and nitrogenous waste products like blood urea nitrogen and creatinine are retained in the body when someone has AKI, a syndrome. One of the frequent and serious syndromes seen in clinical practise is AKI. Gastroenteritis is an inflammation of the small intestine and stomach that causes diarrhoea, vomiting, and nausea. In India, diarrheal illnesses constitute a significant public health issue.

Furthermore, Pre-Renal Azotaemia 58%, followed by acute Tubular Necrosis in 42%.This is not similar to a study by Shah et al., [8], that reported Acute Tubular Necrosis in 54% followed by Pre-Renal Azotaemia 46%.

Moreover, 42% of patients were in the age group of \(55->65\) years, 36% of patients were in the age group of 25-44 years. This differs from studies of Feest et al., [9], where the Majority of the people were more than 60 yrs, and 48% of ARF cases occurred in patients over 65 yrs in a study by Liaño et al., [10]. This implies the occurrence of AKI more in younger age groups, also observed in other studies. This is mostly related to factors encountered in the environment and exposure due to work-related activities [11].

A study by Pajai et al., [12] demonstrated the major complications noted were hypotension in 32 patients (60.4%), sepsis in 29 patients (54.7%), and multiorgan failure in 9 patients (16.9%), encephalopathy in 4 patients (7.5%), and ARDS 3 patents (5.66%). Inbanathan et al., [13] recorded hypovolemic shock (61%), anemia (19%), pulmonary edema (14%) metabolic encephalopathy (7%) as complications.

Twenty patients in the ATN group saw improvements after receiving conservative care. The ATN group's 34 patients required hemodialysis. None of the 46 patients in the Pre-renal group required hemodialysis since they all responded to conservative treatment. Sixty-six of the 82 patients who lived made improvements with conservative therapy, while sixteen needed hemodialysis.

A study by Shah et al., [8] reported at admission. The mean urea concentration was 150.51 mg/dl with a range of 30 to 401 mg/dl. A mean peak urea level of 166.24 96.14 was recorded. At the time of discharge, the mean urea level was 81.89 61.92. The mean baseline urea level in survivors was 134.75 88.79, while it was 222.32 95.35 in non-survivors. Hyponatremia (145 meq/L) was present in 27 patients (27%) of whom 3 were admitted and the rest were hospitalized.

In Mc Murray's study, 74% of ATN patients had infections. In their study, the urinary tract was the site of infection most frequently (20%), and 7 patients (14%) had septicemia. The incidence of oliguric renal failure reported by Anderson et al., [14] was similar (9%) in this case. In our study, UTI (%) and the lungs were the most commonly infected areas, and 11 patients developed septicemia.

In our study, the most common complication was septicemia was observed. Cardiovascular complications were 43% in Minuth et al., 13 study [15]. Neurological complications were 38%, and Pulmonary complications were 28% in Anderson et al., [14] 12 study.

Oliguria, persistent hypotension, and coma were all found to be substantially linked with greater mortality in our study. In our study, mortality was 16% overall, with the ATN group accounting for the majority of deaths. It is considerably lower than in earlier research. In the prerenal and intrinsic groups of ARF, it was 10.3% and 23.8%, respectively; in a research by Kaufman et al., [16] 60% mortality in the ATN group and 45% overall mortality were reported.

In the pre-renal and ATN groups, the time from the onset of gastroenteritis and the development of AKI was practically comparable, and no statistical difference was found. Age alone has been linked in certain studies to the outcome of AKI, however other investigations have found that age alone is not a predictor of AKI. Given that our study only included a small number of patients who fell within a specific age range, it is not reasonable to draw the conclusion that age and sex are independent predictors of the outcome of AKI.

In our study, there were 15 patients with non-oliguric renal failure (30%), and none of them passed away. The fact that 10 of the 42 oliguric and anuric patients died compared to 10 of the 15 non-oliguria patients suggests that the urine output may be one of the predictive indicators for AKI brought on by gastroenteritis.

7. Limitation

This is a single-center study, and the limited number of patients. Despite the limited sample size, however, the post hoc power of our study is acceptable. Another limitation was that it was not possible to use the KDIGO urinary output criteria, which could have determined underestimation of AKI prevalence.

8. Conclusion

One of the main causes of AKI, gastroenteritis, accounted for 16% of all patient deaths who had AKI in our study. The 50 patients had an ATN diagnosis in 42% of cases and pre-renal azotemia in 58% of cases. 30% of the patients weren't oliguric at admission, 20% had anuria, and 50% of the patients had oliguric symptoms. The most frequent complication, which affected 8 patients, was septicemia. All of them passed away. Due to the frequent incidence of hypokalemia, ARF brought on by gastroenteritis differs from other ARF and has a better prognosis. An significant electrolyte disruption in AKI brought on by gastroenteritis is hypokalaemia. It was determined that the primary factor leading to death in AKI caused by gastroenteritis is septicemia.

Author Contributions:

All authors contributed equally to the writing of this paper. All authors read and approved the final manuscript.

Conflicts of Interest:

''The authors declare that they do not have any competing interests.''

1. Introduction

A wake craniotomy can be defined as a neurosurgical procedure performed while the patient is awake and alert during surgery. Awake brain surgery is used to treat brain tumors, epileptic seizures near areas that control language, movement or cognition, movement disorder, and recently during neurovascular surgery [1]. When the patient is alert, we can ask questions and request specific movements or responses from the patient so we can monitor brain performance as we operate; this can help ensure the brain remains safe while the tumor is removed.

Early in its history, awake Craniotomy was used to treat epilepsy. The modern era of awake craniotomies began in the late 1920s when Wilder Penfield was attempting to treat patients with intractable epilepsy; Archer, in 1988 first surgeon who performed awake Craniotomy for brain tumors [2, 3]. This procedure has become increasingly popular with broader indications prompted by evidence that patients receiving awake Craniotomy have better outcomes in many aspects.

The improvements in anesthetic agents and techniques, the application of neuro-navigation, and intraoperative electrical mapping are reliable methods to minimize the risk of the permanent deficit during surgery for brain tumors in eloquent areas [3].

2. Indications and contraindications

There are many indications for awake craniotomy. For neuro-oncology, the resection of any intra-axial masses that are near eloquent areas can benefit from awake surgery, as the patient monitoring and the brain mapping that we perform in these surgeries enable us to resect more of the tumor without injuring the cortical centers and subcortical tracts with less risk of post-operative neurological morbidities when we compare it to general anesthesia [4, 5]. Furthermore, as the extent of resection of the lesions in neuro-oncological surgeries is directly correlated to the survival and quality of life in many tumors, awake craniotomy can be superior to classical surgeries. In particular cases, in patients with specific skills like musicians, we perform functional MRI to localize the musical perception area and the relation with the tumor to resect the lesion without disturbing the musical ability. It is an individually tailored mapping.

In epilepsy surgeries, in the case of drug-resistant seizures where the foci are extra temporal, resection becomes difficult, as they are closer to the eloquent cortex in most cases. These cases benefit from awake craniotomy as mapping the cortex before resection protects the critical areas and makes the surgery safer.

Also, the utility of awake surgeries in some neuro-vascular procedures, awake surgery during aneurysm clipping to prevent ischemic episodes during temporary clipping [1], and endarterectomies, where the frequent examination of the patient while clamping the diseases carotid to perform the surgery can show the examiner the dependency of the patient on that particular vascular axis, and help the surgeon chose the proper surgical technique (shunting vs no shunting). Another benefit that can push the surgeon to go for awake surgery to prevent the risks of general anesthesia may prevent extended hospitalization and ICU stay. Also, it will help the anesthesiologists use less invasive methods and catheters to monitor the patients.

On the other hand, there are many factors that contra-indicate awake surgeries. The most important one is patient cooperation, as cases of agitation or non-cooperation while performing the surgery can lead to dangerous outcomes and injuries. This makes patient selection very important. No clear consensus on the proper age for awake surgeries, as they were performed on pediatric and geriatric patients. Patients with difficulty talking, who are somnolent or confused due to some tumor, may not benefit from awake surgery even if its location is ideal due to the impossibility of performing pre-op examinations. Furthermore, long surgeries with heavy blood losses and uncomfortable positions make a relative contra-indication to awake surgery as they can lead to agitation and non-cooperation. Obesity, sleep apnea, and other conditions that can lead to insecure airway stability can cause a relative contra-anesthesia in Awake craniotomy.

3. Preoperative preparation

Awake craniotomy requires a highly cooperative patient and an expert surgical team. Preoperative airway evaluation should be performed in all patients. Control of preoperative anxiety before awake craniotomy is important and can be relieved by proper preoperative counseling about the anesthetic and surgical procedures. Therefore preoperative consultation by an anesthesiologist is a necessary process. The anesthesiologist should outline the overall awake craniotomy procedures, including positioning, scalp nerve block, possible discomfort, and the motor and language test. A good anesthesiologist-patient relationship is essential, and the anesthesiologist should attempt to alleviate the anxiety and discomfort of the patient.

4. Anesthetic approaches for awake craniotomy

Various anesthetic techniques may be helpful for awake craniotomy. Among them are two commonly used anesthetic methods for awake craniotomy: monitored anesthesia care (MAC) and the asleep-awake-asleep (AAA) technique. The anesthesiologists should provide sufficient sedation and analgesia during the initial craniotomy; rapid and smooth emergence of patients is required for the intraoperative neurophysiologic test, including motor and language tests and brain mapping.

After the tumor resection, sedation is often sufficient until the completion of the surgery. The sedation profile during the first stage of awake craniotomy, from scalp incision to dura opening, plays a pivotal role in the quality of intraoperative consciousness. The anesthesiologist should restore the patient's consciousness to the preoperative state for neurophysiologic tests and brain mapping to be performed successfully.

In our institution at Mount Lebanon hospital-Balamand university hospital, the combination of propofol and remifentanil has been considered the standard protocol for sedation during the first stage of awake craniotomy because of the ease of use and reliability. The propofol and remifentanil-based AAA technique allow a smooth emergence and rapid recovery of consciousness for intraoperative neurophysiologic testing. The propofol and remifentanil-based MAC technique is associated with dose-dependent respiratory depression, which can produce hypercapnia and subsequent brain edema. Therefore, achieving the optimal sedation level for an individual is crucial. Meanwhile, light sedation risks causing accidental patient movement, and anxiety is likely. Generally, drowsiness but readily responsive state is considered the optimal sedation in awake craniotomy, and experienced anesthesiologists are required to accomplish this balance in the complex setting.

Dexmedetomidine, an alternative to propofol for the MAC technique during awake craniotomy, can also be used. It is a selective alpha-2 agonist with sedative, analgesic, anxiolytic, and sympatholytic properties. The advantageous effects of dexmedetomidine, such as minimal effect on neurophysiologic monitoring, stable hemodynamics, and minimal respiratory depression, make it suitable for sedation during awake craniotomy. Dexmedetomidine and the scalp nerve block were used successfully in awake craniotomy, but it can cause bradycardia, that's why it needs good dose monitoring techniques.

Anesthesia for awake craniotomy is one of the most challenging fields for anesthesiologists. The MAC and AAA techniques are feasible and safe anesthetic techniques for awake craniotomy, and an adequate regional block is required for effective intraoperative pain control and better patient satisfaction. Appropriate patient selection, perioperative psychological support, and proper anesthetic management for individual patients in each stage of surgery are crucial for procedural safety, success, and patient satisfaction.

5. Pre-operative planning

The neuro-onology multi-disciplinary team meeting should discuss most awake craniotomies for brain tumor resection. Good radiological imaging should be done for surgical planning, including diffuse tensor imaging (DTI) if the tumor. In addition, a formal speech and motor power assessment evaluation is usually carried out up to 2 days before surgery (baseline) and repeated intra-operatively to identify errors during stimulation. Although fMRI is increasingly being adopted as a practical preoperative planning tool for brain tumor resection, there remains a substantial discrepancy about its current use and presumed utility.

In a comprehensive neuropsychological evaluation, a patient's emotional state and ability to cooperate during awake surgery are usually assessed, and meeting the team before surgery is crucial as well. Indication, and so a proper evaluation by the anesthesiologist pre-op should be performed.

Surgical Technique As with any awake technique, delays and technical problems in the operating theatre should be avoided. The team should be aware of the presence of an awake patient by a sign on the entrance of the operating room, and noise should be kept to a minimum. The operating theatre becomes crowded, staff movement should be restricted, and a calm atmosphere should be maintained at all times. Patient comfort is essential. We should ask the patient if they are comfortable, the operating table should be adequately padded, and attention should be paid to head and limb positioning. That should be double-checked before draping the patient. It is usually preferable to allow the patient to position themselves on the operating table before the institution of sedation or anaesthesia to lie in the most comfortable position. If a Mayfield head fixator is used, adequate local anaesthesia should be applied prior to application of the pins. Surgical drapes should be positioned, allowing the anaesthetist constant and unimpeded access to the airway while preserving a sterile field. The use of transparent drapes reduces the feelings of claustrophobia.

Whether sedation or an asleep-awake-asleep technique is chosen, it is crucial to apply adequate local anaesthesia on the skin incision called elliptic block, using combinations of lidocaine and bupivacaine with epinephrine. The skin, scalp, pericranium, and periosteum of the outer table of the skull are all innervated by cutaneous nerves arising from branches of the trigeminal nerve; subcutaneous infiltration with local anaesthesia in the manner of a field block or over specific sensory nerve branches blocks afferent input from all layers of the scalp.

The skull can be drilled and opened without pain or discomfort to the patient since there is no sensory innervation. However, the dura is innervated by branches from all three divisions of the trigeminal nerve, the recurrent meningeal branch of the vagus, and branches of the upper cervical roots [1]. Usually, in most brain tumor surgery, we use neuro-navigation to minimize the incision size and identify the vascular anatomy and cortical anatomy.

Functional neuroimaging has improved the pre-planning of surgery in eloquent cortical areas but remains unable to map white matter. Thus, tumor resection in functional subcortical regions still presents a high risk of sequelae. The authors successfully used intraoperative electrical stimulations to perform subcortical language pathway mapping to avoid a definitive postoperative deficit. They correlated these functional findings with the anatomical location of the eloquent bundles detected using postoperative MRI [4, 5].

6. Awake phase

The goal is to transition smoothly and rapidly without agitation, confusion, or drowsiness from sedation or anesthesia to an awake patient. The patient needs to be engaged, cooperative, pain-free, and comfortable for mapping and tumor resection. All agents are stopped; I prefer to keep the patient awake. Pain should be managed with supplemental Local aesthesia. Non-pharmacological intraoperative management should be used to reduce fear and anxiety. Empathy, handholding, reassurance, ongoing encouragement, coaching, and conversation are all useful and important. A sponge soaked with ice-cold water can be used to wet the patient's lips and mouth for comfort. The patient can be allowed to move limbs and hips at appropriate times. An air blanket is used to provide either warm or cool air to maintain a comfortable temperature [6, 7, 8].

7. Physiological test

8. Motor and sensory pathways

Awake surgery accurately maps both cortical and subcortical pathways of the limbs, face, and mouth. Mapping can elicit or inhibit movements. Responses of orofacial musculature, laryngeal activity, and vocalizations can be recorded as tingling or movement, for example, withdrawal of protruded tongue or speech arrest [6, 9]. Similarly, tingling, twitching, or movement in the limbs may be elicited, most commonly in arms and hands [8, 10]. The anesthesiologist should observe the patient and report every movement to the surgeon. That is why the anesthesia team should examine the patient before surgery, and the patient should also be instructed to report any abnormal movement or sensation. The stimulation mapping not only delineates the cortical areas but also allows the surgeon to stimulate and monitor subcortical tracts.

9. Language

It is not easy to localize speech areas based on anatomical landmarks. To assess speech, the Visual Object Naming Test is frequently used. The Boston Naming Test consists of 60 drawings of everyday objects graded in difficulty, for example, window, car, dog, and guitar [11]. In addition, language functions can be studied with more terrific refinement and complexity. Bilingual patients need to be tested in both languages, as the anatomical areas may not entirely overlap. Classic models of language organization posited that separate motor and sensory language foci existed in the inferior frontal gyrus (Broca's area) and superior temporal gyrus (Wernicke's area), respectively, and that connections between these sites (arcuate fasciculus) allowed for auditory-motor interaction. These theories have predominated for more than a century, but advances in neuroimaging and stimulation mapping have provided a more detailed description of the functional neuroanatomy of language. New insights have shaped modern network-based models of speech processing composed of parallel and interconnected streams involving both cortical and subcortical areas. Recent models emphasis-size processing in "dorsal" and "ventral" pathways, mediating phonological and semantic processing, respectively; phonological processing occurs along a dorsal pathway, from the posterosuperior temporal to the inferior frontal cortices. On the other hand, semantic information is carried in a ventral pathway that runs from the temporal pole to the basal occipitotemporal cortex, with anterior connections.

10. Visual

Intraoperative brain mapping of the cortical visual cortex with subcortical mapping of visual tracts may be useful to minimize the risk of permanent hemianopia in tumors located in the parieto-occipital area. Identifying optic radiations by direct subcortical electrostimulation is a dependable method to reduce permanent injury in surgery for gliomas involving visual pathways [11, 12]. In addition, methods to identify other functions, such as memory and counting, are of interest and are being developed.

11. Challenges during the awake phase

The main challenges during awake craniotomy include: hypertension, seizures, somnolence, agitation, oxygen desaturation, tight brain, and shivering.

1. Hypertension: This is most commonly secondary to pain, agitation, and anxiety. However, other causes should also be sought such as hypoxia, hypercapnia, and dexmedetomidine (DEX) associated [5, 6, 9, 13]. Treatment should focus on managing the cause. Labetalol or esmolol may sometimes be necessary.
2. Seizures: Seizure incidence is 3\% to 16\% and happens during cortical and subcortical stimulation mapping [14, 15]. If the surgeon avoids stimulating an area twice in rapid succession, the incidence is less. Continuous monitoring of electrocorticography for spikes or sharp waves within 5 seconds after each stimulation allows early detection [17]. Patients with a history of seizure and younger patients, especially with tumors of the frontal lobe, are more prone to seizures [17]. Intraoperative seizures have a higher incidence of transient motor deterioration, and longer hospitals stay [11, 16]. First-line treatment of stimulation-evoked seizures is irrigation of the cortex with a cold crystalloid solution, which can be repeated as often as necessary.
3. Emergence agitation and delirium may occur if the pre-awake phase is with GA or deep sedation. Contributing factors include older age; pain; disorientation; inappropriate use of naloxone, flumazenil, neostigmine, and atropine; oxygen desaturation; hypercapnia; urethral stimulation, and bladder distention. It can be tough to manage, and there is no consensus on the best approach. An approach is to reinduce anesthesia with a propofol bolus, then administer a dexmedetomidine bolus before the second wake-up attempt [10, 18].
4. Somnolence: This usually reflects residual anesthetic effects or from anti-consultants. The best strategy is prevention by early termination of DEX and propofol, and the avoidance of large doses of midazolam or longer acting opioids.
5. Nausea and vomiting: These are most commonly associated with opioids; other common associated factors are age, gender, and anxiety. The incidence is much lower with the common use of propofol. Management includes empathy, ondansetron, and small dose of propofol.
6. Hypothermia and shivering: These should be prevented by the use of blankets, warm air devices, and appropriate room temperature. Tramadol or meperidine may be effective [6]. Post-awake and post operative care.

Suppose we perform an awake-asleep-awake anesthesia type similar to the pre-awake phase. In that case, one can also choose awake, spontaneous ventilation under light or deep sedation, or GA with airway control. Sedation often suffices. The patient usually requires lower rates of sedative infusions during the post-awake phase than during the pre-awake phase, as patients are often fatigued, and there is a lower level of painful stimuli during skull closure. The patient should initially require to be admitted to the neurosurgical intensive care unit, with hourly neuro observation for the first 24 hours. Pain management can be achieved intravenously with small doses of opioids, including with patient-controlled analgesia, and oral opioids combined with anti-inflammatory drugs.

Author Contributions:

All authors contributed equally to the writing of this paper. All authors read and approved the final manuscript.

Conflicts of Interest:

''The authors declare no conflict of interest.''

1. Introduction

The Baricity of bupivacaine is one of the most critical factors in influencing the distribution of the local anesthetic and the spread of the blockade [1]. Bupivacaine is rendered hyperbaric by adding glucose. The effect of differing degrees of hyperbaric remains to be evaluated in terms of spinal anesthesia blockade. The measured sensory blockade and motor blockade are the onset and duration. Duration of sensory block was the time measured from the time of the highest block for the regression to the S2 dermatome.

The aim of this prospective, randomized, double-blinded study was to make a direct comparison between 0.5% isobaric bupivacaine in 80 mg/ml and 40 mg/ml of glucose in terms of spinal anesthesia blockade and that the recovery profile for bupivacaine may be of interest given that more surgery is being performed in the day case setting [2].

Spinal anaesthesia is popular in both small children and older people. Spinal anaesthesia produces rapid onset, profound, and uniformly distributed analgesia with good neuromuscular block. Local amide anaesthetics (bupivacaine) are used regularly, and spinal anaesthesia allows the use of a small dose with a low risk of systemic toxicity. Baricity (weight of anaesthetic solution about the weight of cerebrospinal fluid (CSF)) is one of the most critical factors that influence distribution of local anaesthetic solutions in CSF. Solutions administered most frequently are hyperbaric as they produce a more predictable block in both adults and children [3]. Studies in adults have found that the addition of a small amount of glucose to increase the Baricity of bupivacaine solution just into the hyperbaric range improved the predictability of spinal block [4]. Two different hyperbaric bupivacaine solutions (80 mg/ml glucose and 40 mg/ml glucose) were compared.

2. Patients and methods

Our Ethics Committee approved the study. All patients gave informed consent. We studied 100 patients, ASA I-II, aged 20-60 yr, undergoing day-case surgery below the umbilicuslower abdominal, hips, and lower extremity surgeries ) and were randomized into two groups in a double-blind, randomised, parallel-group, prospective study. Group I received 0.5% isobaric bupivacaine with 80 mg/ml of glucose, while Group II received 0.5% isobaric bupivacaine with 40 mg/ml of glucose. Patients with a known contraindication to spinal punctures, such as increased intracranial pressure, haemorrhagic diathesis, infection at block, or allergy to bupivacaine, were excluded. Data were collected between July 2021 and June 2022. We used a double-blind, randomized, parallel-group, prospective study design. Patients were allocated randomly (computer-generated) to receive spinal anaesthesia . Intraoperative monitoring consisted of non-invasive arterial pressure measurements every 5 min, continuous ECG, ventilatory frequency, peripheral arterial oxygen saturation, and end-tidal carbon dioxide concentration. Appropriate treatment was given if systolic arterial pressure or heart rate decreased to less than 75% of baseline. All adverse effects were recorded. All patients were administered oxygen and monitored closely by the anaesthetist or anaesthetic nurse. Lumbar puncture was performed in the sitting position using a midline approach at the L3-4 or L4-5 interspace. Standard 27-gauge, 90-mm long spinal needles(Pencan). Correct placement was verified by free aspiration of CSF. After injection of local anaesthetic, free aspiration of CSF has verified again, and the patient was placed in the supine, horizontal position. During spinal puncture, the following variables were recorded: interspace used; and time to complete the block. The highest median level of sensory block was T3 (T2-T7) (median (10th/90th percentiles)) in both groups. Time to reach T10 did not differ between the groups. A pinprick testing was used to evaluate the width of the analgesic area 15 min after injection of the anaesthetic. A movement in a rostral direction along the surface of the trunk was used until the patient reported mild pain, indicating the upper border of the analgesic area. The procedure was repeated until the level of the first painful segment was confirmed. Motor block was assessed using a modified Bromage scale recording the patient's ability to flex the ankle, knee, and hip (0=no motor block, 3=complete motor block of the legs and feet). After the operation, patients were transferred to the post anaesthesia care unit (PACU) for continuous monitoring of vital signs and regression of block. Regression of sensory block by two segments was tested every 5 min, and the time was recorded. Patients were discharged when awake, could walk unaided, had stable vital signs for at least one h, had no pain or only mild pain, had no nausea or vomiting, and could tolerate clear fluids. Time to discharge was measured from spinal puncture to actual discharge from the hospital/PACU. Power analysis suggested that a total of 100 adults were required in both groups; 50 patients were required in each group for a 90% chance at the 0.05 level of significance of detecting a 10% difference in success between groups. Categorical data were tested using the chi-square test. For continuous data, the Mann-Whitney test was used. Results are presented as median (10-90th percentiles), number (%) of cases, and the significance was set as \(P< 0.05\).

3. Results

Patient data and the characteristics of spinal punctures were comparable between groups. The success rate of the spinal block was high in both groups, with no differences between groups (Table 1). These results demonstrate that bupivacaine in 80 mg/ml glucose provides reliable spinal anaesthesia with shorter duration and less hypotension than bupivacaine in 40 mg/ml glucose. The recovery profile for bupivacaine may be of interest, given that more surgery is being performed in the daycare setting. One hundred patients were randomized into two groups in a double-blind, randomized, parallel-group, prospective study. Both groups had similar characteristics for a spinal puncture(median 10-90\(^{th}\) percentile) with L3-L4 and L4-L5 levels used for spinal puncture with the dose of isobaric bupivacaine 0.5% of 10 mg and the time for the complete block was 30 sec in bupivacaine 0.5% with 80 mg/ml glucose and 60 sec in bupivacaine 0.5% with 40 mg/ml group. The characteristics of sensory block in the two groups were as follow, the height of sensory block was at T4 in both groups and the regression of block by two segments, the regression of block to T7, and the time to discharge from hospital was shorter in bupivacaine 0.5% with glucose 80 mg/ml group compared to bupivacaine 0.5% with 40 mg/ml glucose group (Table 2). The regression of block by two segments was 63 min in group I and 85 min in group II. The regression of block to T7 was 80 min in group I and 103 min in group II.

Time to discharge from hospital was 237 min in group I and 340 min in group II.

There was no differences between groups in the incidence of adverse effects.

Table 1. Characteristics of the spinal puncture and the success rate of spinal anesthesia in the two groups(number %).

	Bupivacaine in 80mg/ml glucose N=55	Bupivacaine in 40 mg/ml glucose N=52
Interspace used for spinal puncture: L3-L4	20	17
L4-L5	35	35
Time to complete (s)	30	60
Sensory block complete	52	51
Motor block complete	53	52

Table 2. Characteristics of sensory block in the two groups (median(10-90 th percentile)). Times are after spinal puncture.

	Bupivacaine 0.5% with glucose 80 mg/ml N=55	Bupivacaine 0.55 with glucose 40 mg/ml N=55
Height of sensory block (dermatome)	T4(T1-T7)	T4(T1-T5)
Regression of block by two segments (min)	63	85
Regression of block to T7 (min)	80	103
Time to discharge from hospital (min)	237	340

4. Discussion

We have compared the anesthetic effects of isobaric bupivacaine 0.5% in 80 mg/ml and 40 mg/ml of glucose solutions. Thus baricity was the main factor responsible for differences in the spinal block. In agreement with the previous studies, a slightly hyperbaric bupivacaine solution produced a predictable sensory block. However, the spread of the block did not show the narrow range observed in adults [5]. In this study, the success rate of spinal with bupivacaine 0.5% in glucose 80 mg/ml was high to complete surgery [6]. We measured the analgesic area using pinprick testing to assess the height and duration of anesthesia and analgesia. The results of our study confirm our earlier findings that the characteristics of sensory block in the two groups, the height of sensory block, the regression of block by two segments, and regression to T7 plus the time to discharge from hospital was shorter in bupivacaine 0.5% with glucose 80 mg/ml group compared to bupivacaine 0.5% with glucose 40 mg/ml group.

Mild hypotension was reported in 15 patients, and 20 reported shivering, a normal physiological response during spinal anesthesia. These results demonstrate that bupivacaine in 80 mg/ml glucose provides reliable spinal anaesthesia of shorter duration and with less hypotension than bupivacaine in 40 mg/ml glucose. The recovery profile for ropivacaine may be of interest given that more surgery is being performed in the day-case setting.

Author Contributions:

All authors contributed equally to the writing of this paper. All authors read and approved the final manuscript.

Conflicts of Interest:

''The authors declare no conflict of interest.''