No

Septic shock still remains the one of the leading causes of death in hospital patients. Barely more than 50% of the patients with severe sepsis survive their hospital admission. This unacceptable high mortality can only be reduced if there is greater awareness and understanding of the condition .and the knowledge of most effective treatment measures available. Unplanned admissions to the Intensive Care Unit (ICU) and potentially preventable deaths on wards are associated with a failure to institute early preventive conditions. Greater than 40% of the intensive Care Unit admissions are potentially preventable with improved ward care.

Survival of patients with Septic shock appears to be better if shock develops while the patient is in Intensive Care Unit rather than on general ward despite greater severity of illness in the intensive care group [1].This suggests that the closer observation and earlier treatment can influence the outcome of sepsis.

INCIDENCE:

Septic shock is an increasingly common problem. The incidence of sepsis is increasing year by year. The reasons for this increase are that the people are living longer and this aged population are the most vulnerable to sepsis. We are using advanced technology to sustain life and there has been a rise in the number of immunocompromised patients due to aggressive cancer therapy and the increased prevalence of HIV. The widespread use of broad spectrum antibiotics has increased the rate of both antibiotic resistance and nosocomial infections.

A prospective, multicentre, observational study, recently conducted to evaluate the epidemiology of Sepsis and other characteristics of Intensive Care Unit patients in European countries (called the SOAP study) was endorsed by the European Society of Intensive Care Medicine [2]. This observational study showed a marked difference in the frequency of sepsis between countries, and higher frequencies of sepsis were mirrored by higher mortality rates. (Fig.1)

Fig 1: Incidence of Sepsis in European Countries

There was a direct relationship between the number of organs failing and the Intensive Care Unit mortality. Patients with no organ dysfunction on admission had mortality rates of 6% whereas those with four or more organ failures had mortality rates of 65 %. [2] (Fig. 2)

Fig 2: The SOAP study

As compared to the incidence of other pathologies in Europe the incidence of severe sepsis is higher (32%) [2] (Fig 3)

Fig 3: Incidence of different pathologies in Europe

In septic patients, older age, positive fluid balance, co morbid diseases on admission; cancer and cirrhosis are the most important variables of mortality.

DEFINITIONS

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response Syndrome (SIRS). This is characterised by body temperature outside 36oC - 38oC, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3. (Fig 4)

Fig 4: Definitions

There are three recognised stages in the hierarchy of the inflammatory response, with progressively increased risk of organ failure and death. Patients with infections plus two or more elements of the SIRS meet the criteria for sepsis. Those who have end organ failure are considered as having severe sepsis; and those who have refractory hypotension along with the above said criteria are consider to be in septic shock (Fig. 5)

Fig 5:  Definitions

PATHOPHYSIOLOGY:

Sepsis is a complex condition starting from an infective stimulus and resulting in an exaggerated immune response. The inflammatory response that was initiated to fight the infection ultimately leads to damage of various organs thorough out the body.

During the onset of sepsis, the inflammatory system becomes hyperactive, involving both cellular and humoral defence mechanisms Endothelial and epithelial cells, as well as neutrophils, macrophages and lymphocytes, produce powerful pro-inflammatory mediators, especially tumour necrosis factor- (TNF-), interleukin (IL)-6, IL-1 and IL-8. Simultaneously, robust production of acute-phase proteins, such as C-reactive protein, occurs and humoral defence mechanisms such as the complement system are activated, resulting in production of pro-inflammatory mediators, including C5a, the complement split product. C5a ultimately enhances cytokine and chemokine production. Furthermore, the coagulation system becomes activated through various mechanisms, often resulting in disseminated intravascular coagulopathy.

The hallmarks of the sepsis are excessive inflammation, excessive coagulation and suppression of fibrinolysis. In addition endogenous Activated Protein C which modulates coagulation, controls inflammation and supports fibrinolysis is also decreased. There is considerable variability in response which is almost certainly to a large degree genetically determined. Those with a tendency to produce excessive cytokines and TNF will have a greater inflammatory response. Simultaneously, the initial vascular damage results in neutrophil activation, neutrophil-endothelial cell adhesion, and further elaboration of inflammatory cytokines. In tissues already prone to dysfunctional oxygen uptake and metabolism, this vascular injury promotes further tissue hypoxia through regional hypo perfusion. This uncontrolled cascade of inflammation and coagulation fuels the progression of sepsis, resulting in tissue hypoxia and ischemia with resultant organ dysfunction and death.

DIAGNOSIS:

Diagnosis of sepsis is not easy. Making an early, accurate diagnosis of septic shock is a key to increasing survival rates. The signs and symptoms of severe sepsis may be subtle. Although the components of SIRS are non specific, the combination of suspected infection and the presence of SIRS may help alert the clinician to a possible diagnosis of sepsis. Although hypotension is another clinical sign that may signal the onset of septic shock, patient may present with sever sepsis and clinically significant global tissue hypoxia in its absence. Metabolic marker such as serum lactate, arterial base deficit may help to identify the severe cases. A single lactate measurement of 4mmol/l or more at initial presentation is associated with an increased rate of mortality [3]. There may well be signs of altered mentation and   abnormalities of renal and liver function test, as well as coagulation abnormalities. At least two blood cultures and cultures of other sites as indicated before commencement of antibiotic therapy. Diagnostic studies such as Ultra sound and CT scan should be performed promptly.

D dimmers are grossly elevated in sepsis. Levels of Protein C are lowered which has therapeutic implications. The potential role of biomarkers for diagnosis of infection in patients presenting with severe sepsis remains undefined. Perhaps the most common considerations as diagnostic biomarkers for sepsis have been C-reactive protein and procalcitonin. Despite initial enthusiasm for their potential diagnostic strengths,[4] they have more recently been related to the growing heap of biomarkers that have failed to accurately differentiate sepsis from similar critical illnesses.

The most exciting development in the last 2 years is the recognition of "soluble triggering receptor expressed on myeloid cells-1" (sTREM-1) as a potential biomarker for sepsis. [5] For this marker, a level greater than 60 ng/mL was more accurate than any other clinical and laboratory findings indicating infection

TREATMENT:

The development of new treatment modalities has resulted in a spate of treatment algorithms, often promulgated by medical societies and healthcare improvement organizations. As these modalities have rolled out, increasing levels of evidence have emerged to support or refute their utility in treating patients with sepsis. One of the greatest endeavours to date is the Surviving Sepsis Campaign (SSC) [6] that was originally launched in 2002 with the stated goal to reduce mortality by 25%. The primary method to achieve this goal was the development of evidence-based sepsis care guidelines that were published in 2004. [6] and recently revised in 2008.

The Institute for Healthcare Improvement (IHI) has highlighted sepsis as an area of focus and has identified several deficiencies that may cause suboptimal care of patients with severe sepsis. These deficiencies include inconsistency in the early diagnosis of severe sepsis and septic shock, frequent inadequate volume resuscitation without defined endpoints, late or inadequate use of antibiotics, frequent failure to support the cardiac output when depressed, frequent failure to control hyperglycemias adequately, frequent failure to use low tidal volumes and pressures in acute lung injury, and frequent failure to treat adrenal inadequacy in refractory shock.

The management of patient with sepsis is influenced more by appropriate treatment with antibiotics and fluids than by specific intensive care. Therefore early intervention should never be delayed pending admission to the intensive care unit. The early and aggressive treatment of septic shock has been well documented in the survival sepsis campaign which is based on the best current practice.

The cornerstones of treatment are infection control, haemodynamic stabilization, and modulation of the septic response.

1. Infection Control:

Infection control is vital if the patient is to have any chance of survival. Appropriate broad-spectrum antibiotics must be given within the first hour of recognition of sepsis after obtaining various cultures. Evidence clearly shows that delay or inadequate antibiotic treatment results in poorer outcome. For every hour lost mortality climbs by 9%. [7] 

Initial empirical anti-infective therapy should include one or more drugs that have activity against all likely pathogens (bacterial and/or fungal) and that penetrate in adequate concentrations into the presumed source of sepsis[8] antimicrobial regimen be reassessed daily to optimize activity, to prevent the development of resistance, to reduce toxicity, and to reduce costs

A focus of infection must be sought for and if discovered dealt with immediately. The patient should be evaluated for a focused infection amenable to source control measures including abscess drainage or tissue debridement. One must weigh up the benefits and risks of the particular procedure chosen. If intravascular devices are a potential source, they must be promptly removed after establishing other vascular access. When source control is required, the effective intervention associated with the least physiologic insult be employed (e.g., percutaneous rather than surgical drainage of an abscess)

2. Haemodynamic Stabilization:

In septic shock there is extensive cardiovascular derangement. Hypotension is caused by myocardial depression, pathological vasodilatation and extravasation of circulating volume due to widespread capillary leak. The initial resuscitative effort is to attempt to correct the absolute and relative hypovolemia by refilling the vascular tree. There is no evidence to support one type of fluid crystalloid or colloid is superior to the other. There is good evidence that early gold directed aggressive volume resuscitation improves outcome of sepsis[9] During the first 6 hours of resuscitation the goals of initial resuscitation are a Central venous pressure of  8-12 mm Hg, Mean arterial pressure (MAP) ≥ 65 mmHg, Urine output ≥ 0.5 mL • kg-1 • hr and a  central venous (superior vena cava) or mixed venous oxygen saturation ≥ 70% or ≥ 65%, respectively The Rivers study clearly shows a reduction in  hospital mortality, 28 day mortality as well as 60 day mortality attributed to the Early Goal Directed Therapy (EGDT) [10]. Early goal-directed resuscitation has been shown to improve survival for emergency department patients presenting with septic shock in a randomized, controlled, single-centre study.[11] Resuscitation directed toward the previously mentioned goals for the initial 6-hr period of the resuscitation was able to reduce in hospital, 28-days as well as 60 days mortality rate (Fig. 6).

Fig 6: Results of Early Goal Directed Therapy (EGDT)

If Scvo2 or SVo2 of 70% or 65%, respectively, is not achieved with fluid resuscitation to the central venous pressure target, then transfusion of packed red blood cells to achieve a hematocrit of ≥ 30% and/or administration of a dobutamine infusion (up to a maximum of 20 µg • kg-1 • min-1) be used to achieve this goal.

It is important to remember that vasopressors should be utilized not only when fluids fail to reverse hypotension, but also during resuscitation to maintain minimally adequate blood pressure. Traditionally, the use of noradrenalin in patients with shock has been restricted by the fear of excessive vasoconstriction that may result in end-organ hypo perfusion. In the past it was usually given only when other vasopressin agents failed, and thus such patients would be predicted to have a poor outcome. Recent studies indicate that the fear of deleterious effect was unwarranted and that noradrenalin may have a role as a first-line vasopressor agent in patients with septic shock.

Vasopressin should be considered in refractory shock despite high dose conventional vasopressors. Vasopressin is an endogenously produced hormone that is deficient in many patients with septic shock. Exogenously administered vasopressin in physiologic replacement doses may act synergistically with other vasopressor agents, and has been associated with early withdrawal of catecholamine. Most studies have evaluated short-term infusions of vasopressin at 0.08 U/minute or less as add-on therapy in patients requiring adrenergic agents. The results show that starting vasopressin in patients with septic shock increases systemic vascular resistance and arterial blood pressure, thus reducing the dosage requirements of adrenergic agents [12]. These effects are rapid and sustained. Substantial enhancement of urine production, likely due to increased glomerular filtration rate, was shown in several studies. A few studies demonstrated clinically significant reduced cardiac output or cardiac index after vasopressin was begun, necessitating cautious use in patients with cardiac dysfunction.

3. Modulation of Septic Response:

There are a number of ways to modulate the septic response. These includes use of steroids, tight glucose control and the use of Activated Protein C. Septic shock causes adrenal suppression and this can be confirmed by measuring cortisol levels or by using the synacthan test. Compare to placebo, the administration of low dose of hydrocortisone (200-300 mg/day in divided doses) to patients with septic shock decrease there requirements for vasopressors [13] and lowered their mortality rate [14]. Low dose hydrocortisone should only be given to non responders of the synacthan test but in practice all patient receive this treatment until the result of the test are received.  Following the Corticosteroid Therapy of Septic Shock (CORTICUS) study there is now an increasing trend towards restricting the use of low dose hydrocortisone only to patients with refractory hypotension who are already on high doses on vasopressors [15]. The trial did show a faster resolution of septic shock in patients who received steroids but failed to show a mortality benefit with steroids therapy. Close control of blood glucose has been shown to increase survival in critically ill septic patient. When conservative (10 – 11.1 mol/L) glycemic control was compared with tight control (4.4-6.1mmol/L) in a multi centre, randomized controlled trial, tight control lead to a significant reduction in mortality (8% versus 4-6%), p < 0-04 and improved morbidity at 12 months [16]. 

Activated Protein C

Human activated Protein C (APC) is an endogenous regulator of coagulation. In order for protein C in the plasma to become activated, it must combine with thrombin and thrombomodulin along with the endothelial protein C receptor. With endothelial damage this activation does not take place resulting in its deficiency. Therefore APC supplementation is a rational therapeutic option. APC has an important role in the management of severe sepsis. It protects against the disruption of the endothelial cell membrane, improves micro circulatory perfusion, and has anti inflammatory, procoagulant, fibrinolytic and anti apoptotic activity. APC must ideally be started with in the first 24 hours of the onset of septic shock. The Recombinant Human Activated Protein C Worldwide Evaluation in Severe Sepsis (PROWESS) trial found activated protein C to reduce the risk of death among all severe sepsis patients by 20% [17] This study has also recognized the risk of complications specially haemorrhages.

Subsequent studies have shown similar results. “Administration of Drotrecogin Alfa (Activated) in Early Stage Severe Sepsis” (ADDRESS trial) also provides the evidence concerning use of rhAPC in adults [18]. Additional safety information comes from an open-label observational study, “Extended Evaluation of Recombinant Activated Protein C” (ENHANCE trail). [19] The ENHANCE trial also suggested that early administration of rhAPC was associated with better outcomes.

Other beneficial Strategies in Sepsis

Low Tidal Volume Ventilation: using normal or high tidal volume (10-12mls/Kg) ventilation will cause over expansion of the normal lung segments. This will in turn result in inflammatory mediators being released in the lung tissue. The consequences of this are the development of Acute Lung Injury (ALI) or Acute Respiratory Distress Syndrome (ARDS). Therefore it is crucial to use low tidal volume Ventilation (6ml/kg) to keep plateau airway pressure less than 30 cm of water [20, 21]

High volume Haemofilteration: In the past five years, many studies have been conducted to evaluate and demonstrate benefits of increasing the volume of ultra filtration and replacement fluid during Continuous Renal replacement therapy [22, 23] particularly in complex and very severe syndromes such as Severe Sepsis and Septic Shock, associated with or without acute renal failure.

In general, the high-volume approach provides higher clearances for middle/high molecular weight solutes than a simple diffusive transport, Continuous veno venous haemodialysis (CVVHD) or a convection-based transport at lower volumes, Continuous veno venous haemofiltration (CVVH). These solutes seem to be primarily involved in the Systemic Inflammatory Response Syndrome, which characterizes the Sepsis syndrome, and their efficient removal may thus be beneficial. [24]

Alternative approaches have been based on more efficient removal of inflammatory mediators by high cut-off hemofilters, which are characterized by an increased effective pore size. Most commercially available hemofilters do not permit a substantial elimination of cytokines because of the low cut-off point of their membranes. The use of high cut-off hemofilters is a new and effective approach to cytokine removal, but it has potentially harmful side effects, such as the loss of essential proteins like albumin [25]. 

Because the reversibility of this disease and the resultant mortality may be greatest during the earliest stages of presentation, proper sepsis management should not be confined within the walls of an Intensive Care Unit. Specific emphasis on appropriate triage to ensure prompt diagnosis of the high-risk patient is vital to the launch of a coordinated and cooperative effort by the primary treating clinician and the intensivist

Ethical Dilemmas in Septic Shock

Patient with septic shock have a high mortality and as yet there is no predictive scoring system which gives accurate predictions of outcome for individual patient. Survival from an episode and septic shock is dependent on patient’s age, number of failed organs, previous health and the time delay before the onset of medial intervention, as well as the appropriateness and quality of medical care. The resources available to us are not limitless and so difficult decisions  have to be made deciding between the potential benefits for one critically ill patient and need for several less critically ill patients. As an intensivist one must set realistic expectations which must be clearly communicated to the families concerned. As septic shock worsens and fails to respond to all therapy, one must be prepared to limit and withdraw treatment.

REFERENCES

1. Lundberg J, Perl TM. Septic shock: an analysis of outcomes for patients with onset on hospital wards vs. Intensive care units. Crit care Med 1998; 26: 1020-24
2. Vincent JL, Sakr Y, and Sprung CL, et al. Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006; 34:344-353.
3. Shapiro NI, Homel MD, Talmor D, Nathanson LA, Lisbon A, Wolfe RE, et al. Serum lactates as a predictor of mortality in emergency department patient with infection. Ann Emerg Med. 2005; 45: 524-8.
4. Harbarth S, Garbino J, Pugin J, et al. Inappropriate initial antimicrobial therapy and its effect on survival in a clinical trial of immunomodulating therapy for severe sepsis. Am J Med. 2003; 115:529-535.
5. Gibot S, Kolopp-Sarda MN, Bene MC, et al. Plasma level of a triggering receptor expressed on myeloid cells-1: its diagnostic accuracy in patients with suspected sepsis. Ann Intern Med. 2004; 141:9-15.
6. Surviving Sepsis Campaign. Available at:    http:// www.surviving sepsis.org/ Accessed March 6, 2007.
7. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis C guidelines for management of severe sepsis and septic shock. Crit Care med. 2004;32: 858-873
8. Battleman DS, Callahan M, Thaler HT. Rapid antibiotic delivery and appropriate antibiotic selection reduce length of hospital stay of patients with community acquired pneumonia: link between quality of care and resource utilization. Arch Intern Medicine 2002; 162(6):682-8.
9. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003; 31:1250-1256.
10. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-1377
11. Emanuel Rivers. The outcome of patients presenting to the emergency department with severe sepsis or septic shock. Crit Care. 2006; 10(4): 154.
12. Obritsch MD; Bestul DJ; Jung R; Fish DN; MacLaren R. The role of vasopressin in vasodilatory septic shock. Pharmacotherapy.  2004; 24(8):1050-63 (ISSN: 0277-0008)
13. Briegel J, Frost H, Haller M, Shelling G, Kilger E, Kuprat G et. Stress doses of hydrocortisone reverse hyper dynamic septic shock: a prospective randomised double blind single centre study. Crit care Med 1999; 27:723-32.
14. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002; 288:862-871.
15. Sprung CL. Update on clinical trials in severe sepsis. CORTICUS trial. Program and abstracts of the Society of Critical Care department patient with infection. Ann Emerg Med 2005: 45 (524-8).
16. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med. 2006;354:449-461
17. Bernard GR, Vincent JL, Laterre PF, et al. Recombinant human protein C Worldwide Evaluation in Severe Sepsis (PROWESS) study group. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. 2001; 344:699-709.
18. Abraham E, Laterre PF, Garg R, et al: Drotrecogin alfa (activated) for adults with severe sepsis and a low risk of death. N Engl J Med 2005; 353:1332-1341.
19. Vincent JL, Bernard GR, Beale R, et al: Drotrecogin alfa (activated) treatment in severe sepsis from the global open-label trial ENHANCE: Further evidence for survival and safety and implications for early treatment. Crit Care Med 2005; 33:2266-2277.
20. ARDS Network Investigators. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000; 342:1301-1308.
21. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wiedemann HP, Wheeler AP, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006; 354:2564-2575.
22. Piccinni P, Dan M, Barbacini S, Carraro R, Lieta E, Marafon S, Zamperetti N, Brendolan A, D'Intini V, Tetta C, et al.: Early iso-volaemic haemofiltration in oliguric patients with septic shock. Intensive Care Med 2006, 32:80-86.
23. Reiter K, D'Intini V, Bordoni V, Baldwin I, Bellomo R, Tetta C, Brendolan A, Ronco C: High-volume hemofiltration in sepsis. Nephron 2002, 92:251-258.
24. Ronco C, Tetta C, Mariano F, Wratten ML, Bonello M, Bordoni V, Cardona X, Inguaggiato P, Pilotto L, d'Intini V, Bellomo R: Interpreting the mechanisms of continuous renal replacement therapy in sepsis: the peak concentration hypothesis. Artif Organs 2003, 27:792-801.
25. Mariano F, Fonsato V, Lanfranco G, Pohlmeier R, Ronco C, Triolo G, Camussi G, Tetta C, Passlick-Deetjen J: Tailoring high-cutoff membranes and feasible application in sepsis-associated acute renal failure: in vitro studies.Nephrol Dial Transplant 2005, 20:1116-1126.

Obesity has become a major health problem of modern society and increasing globally at nearly epidemic proportions especially in western and European countries ^1,2,3,4.

DEFINING OBESITY

Obesity can be simply defined as a condition in which body fat is in excess beyond a point incompatible with physical and mental health and normal life expectancy ⁵ or as a metabolic disorder that is primarily induced and sustained by an over consumption or underutilization of caloric substrate. There are 2 types of obesity; Android obesity which is truncal distribution of fat associated with high incidence of cardiovascular disorders and Gynecoid obesity where fat is distributed to thighs and buttocks associated with pregnancy and not tightly linked to cardiovascular problems ^{6, 7.}

Indices used to for obesity are Ideal body weight in kilograms (Broca’s Index), and more commonly the BMI or body mass index

( also called Quetelet’s index ).

1) Ideal body weight = height in centimeters - 100 for men ( 105 for women ). Overweightness is 20% more than ideal body weight and morbid obesity is twice the Ideal Body weight.

2) BMI = weight in kgs/ square of height in meters

Prevalence

In the US more than 60 million adults can be classified as either overweight or obese with morbid obesity affecting more than 9 million adults. Approximately 30 – 40 % of females are obese and it is estimated that 50 per cent of women will be obese by 2050. A study looking at trends in pre-partum obesity in nine states of the United States found an increase in pre-partum obesity from 13% in 1993–1994 to 22% in 2002–2003 ⁸.

WHO classification of Obesity ⁹

In the UK, 56% of all women are over the recommended BMI, with 33% of them classified as overweight (BMI > 25) and 23% obese (BMI > 30). The Health Survey of England published in 2002 gives data about the prevalence of obesity in England. Females in the reproductive age group (16 – 44 years) have shown a dramatic increase in BMI. The percentage of women with BMI above 30 increased from 12% in 1993 to 18.3% in 2002. Also alarming is that the percentage of morbidly obese women has doubled in the last decade ¹⁰. The dramatically increasing rate of obesity in the general population also extends to women of reproductive age.

Pathophysiological changes in obese pregnant patient

Obesity compounds most of the physiological changes in pregnancy

Airway - Obesity and pregnancy each increase the chance of difficult airway. Limited mouth opening and limited neck movements are common in obesity. There is narrowing of the pharyngeal opening due to excess adipose tissue and on airway examination, the airway will have more commonly high of mallampati grades. In pregnancy, particularly in pregnancy induced hypertension, the mucous membranes in the airway are oedematous and hence more prone to bleeding. Breast enlargement in pregnancy also predisposes to difficult airway.

Respiratory system – There are significant changes in an obese parturient and most of them are additive. In early pregnancy , in a non obese parturient, even before the uterus is large enough to affect respiratory function, women begin to have a sensation of dyspnea. This sensation likely occurs from the increased alveolar ventilation, probably secondary to progesterone effects on the respiratory center in the brainstem ^11,12. By the fifth month of pregnancy, the growing uterus begin to cause a progressive decrease in expiratory reserve volume (ERV), residual volume (RV) and functional residual capacity (FRC), which at term are about 15–20% less than those of the non-pregnant state¹³. Obesity in non-pregnant subjects is associated with a decrease in expiratory reserve volume (ERV), residual volume (RV) and functional residual capacity (FRC), most likely caused by the added weight of excess fat on the chest and abdomen and decreased chest compliance^{13 – 16}. Eng et al.¹³ showed, however, that obese parturients did not have a significant additional reduction in functional residual capacity (FRC) compared to normal-weight parturients, which might be partially explained by the fact that the study was performed with the parturients in the sitting position. Another possible explanation is progesterone which has a relaxing effect on smooth muscle and decreases airway resistance, thus reducing some of the negative effects of obesity on the respiratory system ^{12, 17}.

Dempsey et al.¹⁸ have showed that excess body weight in obesity increases oxygen consumption and CO2 production in a linear fashion. The work of breathing is increased in obese parturients due to chest wall weight and they typically show a rapid and shallow breathing pattern ¹⁸. This leads in turn to a higher ventilatory requirements and work of breathing ^12,19. The supine, lithotomy, induction of general anaesthesia and especially the Trendelenburg position worsen lung volumes significantly. The funtional residual capacity (FRC) is further reduced and the closing capacity (CC) encroaches on the funtional residual capacity (FRC) resulting in small airway collapse, ventilation perfusion mismatch, shunting and hypoxemia²⁰. These physiologic changes make the obese parturient particularly prone to rapid desaturation, stressing the importance of adequate denitrogenation ('pre-oxygenation') before induction of general anaesthesia.

In non-obese parturients, physiologic changes during pregnancy are thought to protect from obstructive sleep apnea, due to high circulating levels of progesterone, which is a ventilatory stimulant ¹⁸. However, obesity increases the risk for obstructive sleep apnea significantly and this syndrome is not uncommon in the obese parturients. Obesity hypoventilation syndrome (OHS , Pickwickian syndrome ) is seen in 8% of population of obese parturients characterized by morbid obesity, alveolar hypoventilation and daytime somnolence. In response to chronic hypoventilation and hypoxemia, they develop polycythaemia, increased cardiac output, cardiomegaly, pulmonary hypertension and eventually right heart failure. There is a significant increase in morbidity and mortality. They are more to obstructive sleep apnoea. Pulmonary embolism and pneumonia are also common in these patients ²⁵.

Cardiovascular system – Cardiac output increases in pregnancy, with a significant increase in cardiac output, becoming detectable by the third week of pregnancy and a 35 - 40% increase by the end of the first trimester. Cardiac output continues to rise throughout the second trimester until it reaches a level that is approximately 50% more than that in the non-pregnant state. For the remaining pregnancy, cardiac output remains relatively stable around that level. During labour, cardiac output increases further by approximately 10% in the early first stage, 25% in the late first stage and 40% in the second stage. Uterine contractions increase cardiac output by further 10–15% and in the immediate post-partum period the cardiac output peaks at as much as 75% above prepartum values ¹⁹. Obesity increases cardiac output even further because of extra amount of fat. Every 100 g of fat increases the cardiac output by 30–50 ml/min²². Blood volume is increased in pregnancy and even more when pregnancy is complicated by obesity. In non-obese parturients, there is a significant reduction in afterload ²². In obese pregnant parturients, however, afterload reduction may be impaired due to increased peripheral resistance and greater conduit artery stiffness ²³. Additionally, obesity is associated with a higher prevalence of hypertension, diabetes mellitus, hyperlipidemia and poor cardiac function and it is one of the leading risk factors for coronary artery disease and cerebrovascular accidents ²⁴. Due to hyperdynamic circulation, there ensues left ventricular hypertrophy and diastolic dysfunction. Systolic function might remain normal but progressively systolic dysfunction may ensue. Pulmonary blood volume increase due to increased cardiac output. Pulmonary hypertension can develop and is exacerbated by supine position, airway obstruction and hypoxemia can develop. In obesity hypoventilation syndrome, right ventricular failure can develop. Increased number of peripartum cardiomyopathy cases are seen in obese pregnant parturients but it is unclear if obesity is a risk factor ²⁵.

The obese pregnant parturients are at an increased risk of supine hypotension syndrome (SHS) due to compression of major abdominal vessels. This is exacerbated by large panniculus which adds to the uterine compression. Tseuda et al. have reported two cases of sudden death on assuming the supine position in morbidly obese patients ²⁶.

Gastrointestinal system – Obesity further decreases lower oesophageal tone which is already decreased in pregnancy and increase the risk of aspiration of gastric contents and Mendelson’s syndrome ^{27, 28}. Hiatus hernia is increased in obese patients. Roberts and Shirley studied obese and non obese pregnant parturients in labour; the gastric volume in obese parturients is five times greater than in the controls ^29,30,31. Obese population have a higher incidence of diabetes, which can cause delayed gastric emptying, increasing the risk for aspiration. Also, it is well known that obesity predisposes to difficult or failed intubation, both of which are associated with a higher incidence of aspiration.

Others - Gestational diabetes is common. Obesity metabolic syndrome includes dyslipidemia, impaired endothelial function, high blood pressure, increased inflammatory mediators, insulin resistance and hyperinsulinemia even in absence of diabetes ²⁵.

Pharmacokinetics and pharmacodynamics changes

Obesity increases both fat and lean masses; however, the percentage of fat tissue increases more than does the lean mass, affecting the apparent volume of distribution of anaesthetic drugs according to their lipid solubility. Thiopental sodium and propofol dosages are calculated on total body weight (TBW). Benzodiazepine loading doses should be adjusted on actual weight, and maintenance doses should be adjusted on ideal body weight. The loading dose of lipophilic opioids is based on total body weight (TBW), whereas maintenance dosages should be cautiously reduced because of the higher sensitivity of the obese patient to their depressant effects. Pharmacokinetic parameters of muscle relaxants are minimally affected by obesity, and their dosage is based on ideal rather than total body weight (TBW). Minimum alveolar concentration is decreased. Inhalation anaesthetics with very low lipid solubility, such as sevoflurane and desflurane, allow for quick modification of the anaesthetic plan during surgery and rapid emergence at the end of surgery, hence representing very flexible anaesthetic drugs for use in this patient population. Drug dosing is generally based on the volume of distribution for the loading dose and on the clearance for maintenance. In the obese patient, the volume of distribution is increased if the drug is distributed both in lean and fat tissues whereas the anaesthetic drug clearance is usually normal or increased ³². Albumin binding of drugs is unchanged in the obese, but levels of fatty acids, triglycerides, and a1-acid glycoprotein are increased and may influence plasma protein binding. In pregnancy, the volume of distribution is increased, albumin concentration decreased and the renal clearance is increased. Net effect is unpredictable. Pseudocholinesterase levels are decreased in pregnancy.

Local anaesthetic requirements

Lower dose of local anaesthetic is required (less by 25%) when injected neuraxially. Proposed mechanisms are pregnancy induced hormone related changes in the action of spinal cord neurotransmitters, potentiation of the analgesic effect of the endogeneous analgesic systems, increased permeability of the neural sheath ²⁵ and decreased dilution by decreased volume of cerebrospinal fluid (CSF) Hodgkinson et al ³³ have shown an increased cephalad spread of local anesthetics in obese patients. Hogan et al.³⁴ found a lower average cerebrospinal fluid (CSF) volume in obese subjectsI, which could explain the decreased local anesthetic dose requirements due to decreased anaesthetic dilution. Since similar changes were noticed with external abdominal compression and abdominal pressure increases linearly with increased body weight ³⁵, increased abdominal pressure is probably the cause. Some ³⁶ have also attributed the decrease in cerebrospinal fluid (CSF) volume to compression of the dural sac due to engorgement of the epidural venous plexus and increased epidural space pressure, resulting from compression of the inferior vena cava by gravid uterus with redistribution of the venous return from the lower limbs and pelvis. Hogan et al.³⁴, however, suggested that the mechanism by which increased abdominal pressure decreases the CSF volume is probably inward movement of soft tissue (mostly fat) in the intervertebral foramen, which displaces CSF. This hypothesis is based on their findings that the greatest change in CSF volume during abdominal compression was found at sites in which intervertebral foramina were present. Greene suggests that larger buttocks of obese patients place the vertebral coloumn in the Trendelenburg position, exaggerating the cephalad spread of the local anaesthetic ^{25, 37}

Consequences of obesity in pregnancy

Obesity severely complicates pregnancy. It affects both the mother and foetus

Maternal consequences

There is increased risk of gestational diabetes and type 2 Diabetes. There is 3 - 10 fold higher risk of gestational diabetes (type 1 insulin dependent diabetes mellitus)³⁸. Studies have shown when pregnancy is complicated by gestational diabetes, there is a higher risk of developing type 2 diabetes mellitus in later life ³⁹. There is a 2 – 4 fold increased risk of preeclampsia. The risk is almost 5 times greater in the morbidly obese group; typically a BMI > 35 ^{38, 40}. But there is no increased risk of HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome ³¹. Obesity is an independent risk factor for hypertension ⁴¹.

It is reported ⁴² that there is a higher chance of failure to progress, prolonged second stage of labour and a failed induction of labour in obese compared to non obese parturients and this is secondary to soft tissue dystocia. There is a higher risk of instrumental delivery of up to 18% in women with a BMI between 35 and 40 and up to 34% in patients with BMI greater than 40. Also there is an increased risk of failed instrumental delivery leading to caesarean section. There is 3 times higher risk of caesarean section in a obese parturient. This is due to fetal macrosomia, higher risk of shoulder dystocia and/or failed cervical dilatation ^{38, 43, 44}. About two thirds present as emergency caesarean section ⁴⁵. The obese parturient is at a higher risk of having a prolonged incision to delivery time, blood loss greater than 1000 ml and prolonged operative times. There is an increased risk of wound infections and endometritis and dehiscence ^{46, 47}. There is an increased risk of major postpartum haemorrhage. The risk of postpartum haemorrhage rises with increasing BMI and is about 30% more frequent for a moderately raised BMI and about 70% more frequent for a highly raised BMI compared with the normal BMI group ^45,48. There is an increased risk of thromboembolism – obesity and pregnancy are each independent risk factors for deep vein thrombosis. Both pharmacological and mechanical methods should be used for thromboprophylaxis.

Obese women spend an average of 5 more days in hospital resulting in 5 fold increase in cost of care due to potential complications such as wound infections and postpartum haemorrhage ⁴⁹.

Fetal consequences

Maternal obesity is associated with large for gestational age infants. There is increased risk of a macrosomic foetus, independent of maternal diabetes ^{43, 50}. There is an increased risk of shoulder dystocia upto three times more common in the morbidly obese parturients. The risk of foetal macrosomia and shoulder dystocia increases with increase in BMI ⁴⁴.

There is an increased risk of Infant birth defects. Since 1994 a number of studies have shown an association between maternal obesity and infant birth defects. Anomalies include neural tube defects such as anencephaly, anomalies of the heart and intestinal tract, omphaloceles, orofacial clefts, and multiple congential anomalies of the central nervous system ^{( 43, 51, 52 )}.

There is an increased risk of stillbirth, a three times increase in antepartum stillbirth was found in morbidly obese parturients compared with women of normal BMI ^{52, 53}.

Due to the depth of maternal adipose, foetal monitoring by intermittent or continuous Electronic Foetal Monitoring using external transducers may be technically difficult. The use of fetal scalp electrodes and intrauterine pressure catheters to ensure an acceptable standard of fetal monitoring may be needed.

In a study ‘Maternal obesity and pregnancy outcome: a study of 287213 pregnancies in London’ (N J Sebire, et all, International journal of obesity (2001) 25, 1175 - 82 ) complications such as gestational diabetes mellitus proteinuric pre-eclampsia; induction of labour; delivery by emergency caesarean section; postpartum haemorrhage; genital tract infection; urinary tract infection, wound infection; birth weight above the 90th centile, and intrauterine death were significantly higher in obese pregnant parturients than non obese pregnant parturients. However, delivery before 32 weeks gestation and breastfeeding at discharge were significantly less likely in the overweight groups. In all cases, increasing maternal BMI was associated with increased magnitude of risk ³⁸. Weiss et al.⁵⁴ found for nulliparous patients a caesarean delivery rate of 20.7% in the control group compared with 33.8% in the obese and 47.4% in the morbidly obese group.

The Confidential Enquiry into Maternal and Child Health 2004 reported that 35% of all maternal deaths occurring in the triennium 2000–2002 were in obese women with BMI > 30. The most recent CEMACH reports in the United Kingdom reported that obesity was a cofactor in a significant number of the maternal deaths between 2003 and 2005. Twenty seven percent of the women who died had BMI > 30. Of these women, 12% had a BMI between 30 and 34, 7% had values between 35 and 39 and 8% had a BMI of 40 or more. 295 women who died 119 were overweight and 64 of those were morbidly or super-morbidly obese. In 30 per cent of women who experienced a stillbirth or perinatal death, the maternal BMI was recorded at more than 30.

Furthermore, Cedergren et al found a 3 fold increased rate of stillbirths, 5 fold increased risk of preeclampsia and a 3 fold increased risk of caesarean section. The success rate for a vaginal delivery in obese parturient with a previous caesarean section is less than 15% ³⁸.

Anaesthetic management

Obese parturients have severely limited physiological reserve and a higher risk of emergency surgical intervention. Hence the anaesthetic risks increase greatly. Obesity and pregnancy each has multisystem effects, many of which are additive. A thorough understanding of the physiology, associated conditions and morbidity, available options for anaesthesia and possible complications is important.

Senior anaesthetist must be involved early in multidisciplinary approach for patient care as early as 28 weeks of gestation. The preoperative assessment include evaluation of airway, respiratory and cardiovascular system and pregnancy associated problems such as pregnancy induced hypertension, gestational diabetes etc and also should include patient education. An examination of the back should be done.

Airway

The obese parturients need thorough pre-operative assessment for difficult airway as incidence of failed intubation is 8 times higher than non obese patients. In the obstetric population, between one in 280 and one in 750 attempted tracheal intubations fail ⁴⁵, compared to one in 2230 in the general population ^{17, 55,56}. In contrast, the incidence of difficult intubation in obese population, is as high as 15.5% ⁵⁷. Dewan ⁵⁸ found the incidence as high as 33% in morbidly obese parturients. A 6-year review of failed intubations in parturients in a United Kiingdom region reported 36 cases of failed intubation and it was found that the average BMI of these women was 33 ⁵⁷. So it is evident that incidence of difficult or failed tracheal intubation in obese parturients is very high and emphasizes optimal assessment and management of the airway. An airway assessment should include mallampati classification, thyromental distance, neck extension (atlanto-occipital joint extension), mouth opening (vertical dimension). The combination of two tests (mallampatti and thyromental distance), though in a small study of 80 parturients receiving general anaesthesia, has been shown to be 100% sensitive with 70% positive predictor value ⁵⁹. These tests can be done in less than 1 minute; hence they are also useful in an emergency scenario. Other features shown to be of significance are short neck, receding mandible and protruding incisors ⁶⁰. It is of interest to note that neck circumference, not BMI, is more predictive of a difficult intubation in morbidly obese patients ⁶¹. A study has shown a gestational weight gain of more than 15 kgs is associated with three times increase in suboptimal layngoscopic view as compared to that in non obese parturients of the same age ^{57, 62}. This means weight gain in pregnancy should be limited in obese parturients and if an obese parturient presents who has gained more than 15 kgs of weight in pregnancy, she will be more likely to have a difficult airway ⁶². A plan of airway management should be formulated in case of an emergency for all women regardless of the primary obstetric and anaesthetic plan. Although rapid sequence intubation with proper positioning and back up equipment may be adequate for most women, an alternative airway plan should be considered. A history of snoring, diagnosis of sleep apnoea, lack of teeth, and large breasts all increase risk of difficult intubation and awake fibreoptic intubation should be considered in all patients with limited range of neck, head or jaw movements, short neck, neck circumference of 15 inches and above, and mallampati score of 3 and above ²⁵

Respiratory System

Usually a complete history and chest examination and routine investigations including an ECG is adequate for a preoperative anaesthetic fitness. However chest X ray, arterial blood gas, pulmonary function tests can be done to aid further evaluation of respiratory reserve. Measurement of oxygen saturation by pulse oximetry in sitting and then supine can provide evidence of airway closure during normal tidal volume ventilation, thereby identifying candidates for post operative oxygen administration ¹⁷.

Women with obesity are more likely to have obstructive sleep apnoea but the prevalence is unknown in pregnancy. Sleep disturbances and day time fatigue are normal at the end of pregnancy and so obstructive sleep apnoea may go undiagnosed. J Mhyre ²⁵ has suggested women with a BMI > 35, neck circumference of greater than 16 inches, symptoms of suspected airway obstruction during sleep ( include frequent or loud snoring, observed pauses in breathing during sleep, frequent arousals from sleep or arousal with a choking sensation ) should be screened by polysomnography for obstructive sleep apnoea and advised continuous positive airway pressure (CPAP) if required.

If obesity hypoventilation syndrome is suspected arterial blood gas is useful to screen hypoxia, hypercarbia and acidosis and echocardiogram should be done to evaluate cardiac function and patient should be referred to cardiologist ^25,63

Cardiovascular system

Cardiovascular co-morbidities such as hypertension, ischaemic heart disease and heart failure can co-exist in obese parturients. Nearly 40% of the obese population experience angina without demonstrable coronary artery disease ⁶⁴. Pulmonary hypertension can be present. Hence cardiologists should be involved early in the care of symptomatic morbidly obese parturients to investigate and optimise the disease status wherever appropriate ¹⁷. Echocardiogram may be useful.

The obese parturients cannot be accurately stratified for perioperative risk using the usual screening indices such as Goldman’s index etc as obesity and pregnancy are not included as risk factors in these indices and they might be classed in the lower risk group despite having significantly increased risk.

Others

Patients should be assessed for pregnancy associated problems such as pregnancy induced hypertension and gestational diabetes mellitus etc.

Peri-operative issues such as transfers, beds, intravenous access, central venous access, difficulty in measuring non invasive blood pressure, arterial cannulation, different size regional anaesthesia kit should be anticipated, discussed and planned for.

Post operative intensive care management /high dependency care should be sought for. Deep vein thrombosis prophylaxis must be put in place. The management plan should be liaised with whole team including consultant anaesthetists, consultant obstetricians, consultant intensivists, midwives, operating department practioners (ODP’s) and physiotherapists

Analgesia for labour

Each of the risk factors of fetal macrosomia and shoulder dystocia which are increased in obese parturient result in more painful contractions and complicated labour ⁶⁵. Although there are various modalities of pain relief, analgesia using neuroaxial blockade has been shown to be the most effective ⁶⁶. The anticipated technical difficulties should not preclude the use of epidural analgesia in obese parturients. It is been shown effective pain relief during labour can improve maternal respiratory function and attenuate sympathetically mediated cardiovascular responses ^{67, 68}. Available evidence shows that the rate of caesarean delivery does not increase with epidural analgesia during labour ⁶⁶, though obesity increases the need for caesarean section. Hence, placing a functional epidural catheter is advantageous should any operative intervention be required. In addition, epidural analgesia can be extended into the postoperative period where adequate pain relief can optimise care.

The challenges for the anaesthetist should not be underestimated. Technical problems include appropriate positioning of the patient, identification of the midline and epidural space, and dislodgement of catheters ^{45, 69, 70}. The initial failure rate for epidural catheter placement can be very high (42%) ⁴⁵ and multiple attempts of catheter placement are common. Jordan et al. noted 74.4% of massively obese parturients needed more than a single attempt and 14% needed more than three attempts for successful epidural placement ⁷¹. The knee–chest position required for doing epidural in the lateral position is difficult to obtain in the obese. One study has shown that cardiac output decreased more in the lateral decubitus position with maximal lumbar flexion compared with the sitting position ⁷². Moreover, in the lateral position, gravity can drag down the pad of fat obscuring the midline. Another study found the depth of the epidural space from skin to be greater in patients where the epidural was inserted in the lateral decubitus position ⁷³. Overall, the sitting position is preferable and should be used.

Steps and caveats

Early placement and confirmation of optimal epidural analgesia even before onset of labour ( when a term patient presents before labour ) is prudent. This allows sufficient time to manage a failed epidural block ( because not only the incidence of failed initial epidural catheter placement is high in obese parturients, but the incidence of failed epidural during labour due to migration of epidural catheter in the fatty subcutaneous tissues is also high )^{17, 74, 75}. Re-evaluate the airway and cardiorespiratory status. Senior anaesthetist preferably a consultant anaesthetist should be involved. Ensure wide intravenous cannula (preferably 14 or 16 gauge) in place. In case of problems with blood pressure cuff not measuring, cuff can be placed on calf/forearm; will help in getting the trends if no accurate reading. Invasive blood pressure monitoring might be needed. Ensure pulse oximetry monitoring and supplement oxygen by mask if required.

Perform in sitting position. Ensure midline position as even if slight deviation of the midline will lead to exaggerated directional errors due to increased length of epidural space from the skin and hence failure of epidural. Midline might be not possible to palpate, in this case drop a line from C1 spinous process to lower skin crease and this may be guide as a midline. Strapping excess fat away from the midline might be necessary.

If highest points of iliac crests are palpated for the Tuffier’s line then because of fat pads on the sides, higher spaces might be inadvertently selected and increased chance of spinal cord damage. In case of difficulty, lower thoracic space may be selected.

A recent study in pregnant patients has shown a positive correlation between BMI and the distance to skin to the lumbar puncture ⁷⁶. Although the epidural space may be deeper in overweight people, the majority of studies report that only a few have an epidural space deeper than 8 cms ^{73, 77}. Hence it seems appropriate to use a standard needle to identify the epidural space on the first attempt. In morbidly obese patient ultrasound technique has been found valuable in establishing epidural ^{78, 79}

In case of difficulty in insertion, a deliberate spinal with 25 guage needle might be performed ( no injection of drugs ) to assess the midline and depth of epidural space. There is an increased risk of dural tap ²⁵, but decreased risk of postdural puncture headache ⁷⁵. In case of dural tap, epidural can be converted to continuous spinal catheter analgesia with extreme caution. Also there is an increased risk of Intravenous placement of epidural catheter due to engorged epidural veins and decrease in epidural space. The meniscus drop ( negative pressure ) test is not reliable as epidural pressure may be high ²⁵. Minimum 5 cms of catheter in space should be left. To minimize catheter displacement, it should be secured on assumption of upright or preferably lateral position from the initial flexed position. The epidural should be checked with a test dose and a functioning epidural should be ensured. Sometimes a longer epidural needle might be required. There is an advantage to titrate block height. Minimum local anaesthetic concentration ( MLAC ) is lower in obese pregnant patients compared to non pregnant patients ⁸⁰

If epidural is contraindicated or impossible to site then entonox is an useful adjunct. Intramuscular opioids are not reliable. Patient controlled analgesia can be used but cautiously as increased chance of sedation and respiratory depression. Remifentanyl, an ultra short acting opioid, has favourable pharmacokinetics to be used as an opioid for patient controlled analgesia but not enough data is available for its use in obese parturients. It is metabolized by red blood cells and tissue esterases both in mother and foetus and hence does not accumulate and is easily antagonized if required. However it is a potent respiratory depressant and hence should be used very cautiously in obese parturients who would be susceptible to its sedative side effects and hence they should be managed in high dependency unit with appropriate monitoring and one to one nursing by skilled midwife and under observation of a highly skilled anaesthetist. The dosage should be carefully titrated individually and naloxone and difficult airway trolley ready. Patients with obstructive sleep apnoea would be very susceptible to its sedative side effects and hence should be avoided. Proper training of patients is required as its peak effect is 2 -3 minutes and if the button of patient controlled analgesia is pressed at the onset of contraction it would be less effective. The duration of its use should be minimized as much as possible.

Analgesia/anaesthesia for Caesarean section

Obesity and Caesarean section have been identified as independent risk factors for maternal morbidity and mortality ⁴⁴. Analysis of direct maternal deaths due to anaesthesia, in the confidential enquiries report on maternal mortality in the United Kingdom from 1979 to 2005, reveals that the majority of deaths occurred under general anaesthesia, compared with regional anaesthesia ¹⁷. Most parturients who die of complications of general anaesthesia die of airway management problems, including aspiration, failed intubation, inadequate ventilation, and respiratory failure.^{54, 55}

Factors that play a role in general anaesthesia being more likely to be associated with maternal mortality than regional anaesthesia are unexpected airway difficulties, pulmonary aspiration of gastric contents, emergency general anaesthesia (including conversion of a failed regional), peripartum haemorrhage, and embolism necessitating general anaesthesia, and resident lack of experience in general anaesthesia for caesarean section ^{28 , 81}.

In Why Mothers Die 2000–02, 35% of all the women who died were obese, 50% more than in the general population ⁸².

Direct maternal deaths due to anaesthesia by types of anaesthesia in United Kingdom 1979–2005. Derived from CEMD reports. Since 1979, maternal deaths are reported as direct and indirect.

GA, general anaesthesia; RA, regional anaesthesia; Other – eg Central VP line insertion

Hence regional anaesthesia preferably epidural should be opted unless contraindicated or difficult.

Regional anaesthesia for Caesarean section

Different techniques can be used. Epidurals are reliable but have high failure rate, spinal is a familiar technique while combined spinal epidural has minimal side effects such as headache, high block , hypotension and can be used post operatively as well as for redo surgery.

Use 25% less local anaesthetic dose compared to non obese patient due to altered neuro-axial physiology and anatomy.

Epidural

A working epidural as above can be continued for caesarean section and it also provides post operative pain relief. However it may be inadequate in more than 25% of these patients, mainly because of difficulty in blocking the sacral roots, resulting in visceral pain upon stimulation of the bladder ⁸³.

Spinal

An obese woman is a candidate for spinal anaesthesia if the airway examination is normal, cardiopulmonary derangements are minimal and the obstetricians aim to complete the surgery within 90 minutes ²⁵. In obese parturients spinals can be technically difficult requiring varied needle lengths and being unable to titrate to block for surgery and surgical duration. If the spinal wears off, general anaesthesia with all its inherent risks, will be required. Tuohy needle can be used as an introducer for the spinal needle ²⁵. Spinal opioids can provide post operative analgesia but respiratory monitoring becomes essential.

Combined Spinal Epidural

Success of combined spinal epidural will depend on familiarity with technique. It is more versatile to titrate the block and dose and also a faster onset compared to epidural alone. This technique can be useful for post operative analgesia and re-operative anaesthesia ⁸⁴. There is higher rate of success for surgical anaesthesia compared to spinal or epidural alone. Several studies have shown that catheters inserted as a part of combined spinal epidural technique produce anaesthesia /analgesia more reliably than those inserted via a standard epidural technique ^{85 – 88}. The appearance of cerebrospinal fluid indirectly confirms correct epidural needle placement and increase the chance of functional epidural catheter. There is a possible flaw when spinal injection alone produces the desired block and epidural remains untested; when epidural is required and fails, general anaesthetic might be needed ²⁵ and hence a small dose intrathecally might be used to establish the analgesia to make mother pain free (which therefore also decreases the risk of hypotension) and then epidural should be used to make sure it is working for the complete surgical anaesthesia.

Continious Spinal anaesthesia

Operators need to be familiar with technique. Continuous spinal anaesthesia must be done always with consultant anaesthetist. It is occasionally used in patients who have accidental dural puncture. It may be used when epidural is indicated and difficult to site. It provides reliable and predictable block and allows to titrate the block to desired level and duration. It provides surgical anaesthetic level within minutes in emergency situations with incremental doses. It is important to flush the catheter before placement to avoid introducing air into the spinal space which could cause pneumoencephalus headache ²⁵. It is also very important to mark it as an intrathecal catheter and to be used by anaesthetist only. This can be used for analgesia as well as anaesthesia.

Incidence of headache and infection is higher with this technique compared to other regional techniques but overall incidence of post dural puncture headache in obese parturients is lower ^{89, 90}. Final density and level are proportional to the dose in mgs, not the volume delivered

General anaesthesia for Caesarean

Consultant anaesthetist should be involved as early as possible. Strategy should be to avoid need for emergency general anaesthesia by being proactive and establishing effective regional analgesia and anaesthesia as early as possible. Airway assessment regarding difficult airway must be done. Preparation for general anaesthesia and difficult intubation (ensure lower sized endotracheal tube and a laryngeal mass airway) must be in place including awake fibre optic laryngoscope. Anti-aspiration prophylaxis must be given before conduct of anaesthesia

Collins et al. ⁹¹ investigated the effect of the position of the patient on the view obtained during laryngoscopy in 60 morbidly obese patients. They found that the 'ramped' position, accomplished by arranging blankets underneath the patient's upper body and head until horizontal alignment is achieved between the external auditory meatus and the sternal notch, clearly improves the laryngeal view when compared with the standard 'sniff' position. HELP (Head elevated laryngoscopy position) should be given to make sure that airway is in alignment.

After all monitoring including foetal monitoring is in place, patient must be prepared awake and draped. Adequate preoxygenation { 8 vital capacity breaths of 100% oxygen ⁹²} is ensured as otherwise they rapidly desaturate. Baraka et al. ⁹² showed that pre-oxygenation achieved by eight vital capacity breaths within 60 s at an oxygen flow of 10 liters/min not only results in a higher partial pressure of arterial oxygen (PaO2), but also in a slower hemoglobin desaturation when compared with the four deep breaths technique. Use standard rapid sequence induction with cricoid pressure and left lateral tilt in patients with no anticipated difficult airway. For general anaesthesia make sure drug doses for (thiopentone, suxamethonium, atracuruim) are calculated before hand keeping in view altered distribution and elimination in obese patients. Dewan suggests that at least 4 mgs/kg of thiopentone (up to a maximum dose of 500 mgs) should be used if chosen, to avoid the risk of maternal awareness, hypertension and decreased uterine blood flow during light anaesthesia ⁹³. Administration of a larger dose may be associated with delayed arousal in the event of failed intubation. For suxamethonium, dose based on 1 - 2 mgs/kg of actual bodyweight up to maximum of 200 mgs ⁹³.

Tracheal intubation should be confirmed by capnography in addition to auscultation. Endobronchial intubation should be promptly recognized and managed. In the event of failure to intubate the trachea after rapid sequence induction, it is imperative to institute a failed intubation drill without delay. Repeated attempts and a second dose of suxamethonium are seldom beneficial and often detrimental. The primary objective in the management of failed intubation is to ensure adequate maternal oxygenation despite the concerns of foetal wellbeing or risk of regurgitation ¹⁷.

Patients will need suitable ventilators for adequate ventilation. They need large tidal volumes of 10–12 mls/kg and positive end expiratory pressure (PEEP) may be avoided ²⁵, as though it increases partial pressure of oxygen in blood ( PaO2 ) ²⁵, it might decrease cardiac output and oxygen delivery to foetus ²⁵. Extubation must be done when awake in left lateral position or semi upright position after adequate reversal of muscle relaxant

Antibiotic prophylaxis is a must as high incidence of wound infection in these patients ^{46, 47}. There is increased risk of post operative respiratory failure and hence morbidly obese parturients are best managed in intensive care management or high dependency care post operatively after general anaesthesia ⁷⁵. Adequate pain control (Patient controlled analgesia / patient controlled epidural analgesia ( PCA/PCEA) to assure post op deep breathing. Infiltrative analgesia at the end of surgery can be carefully used to decrease requirement of post op analgesia. Post operative oxygen should be given and continuous positive airway pressure if required.

Thromboprophylaxis should be given after liasing with the obstetricians as to the dose and frequency required. Both pharmacological and mechanical methods and early mobilization should be used for thromboprophylaxis. It has been suggested that low molecular weight heparin (LMWH) dosing should be based on actual body weight ⁹⁴.

The anticoagulation status of the patient becomes particularly important for the anesthesiologist when the patient has a spinal or an epidural catheter. According to European guidelines (when a single daily dosing of low molecular weight heparin (LMWH's) is used), catheters can be removed 10–12 hrs after the last dose of low molecular weight heparin (LMWH) and 4 hrs before the next dose.

Subcutaneous and Intramuscular routes of drug administration should be avoided as they are less reliable.

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