Essay: Critical incident analysis: rapid deterioration of a burns patient with sepsis

A critical incident analysis is a valuable learning tool enabling nurses to reflect and deal with challenging situation. Reflecting on everyday practive enables us to learn and evolve our practice from both positive and negative experiences and situations.
My essay will analyse the rapid deterioration of a burns patient with sepsis occurring immediately after showering.
The early identification and management of a deterioreting patient is vital. Anticipation and responsive monitoring can considerably reduce complications. As Dagmar Luettel, Kate Beaumont and Frances Healey suggest 23,000 in- hospital cardiac arrsts could be avoided annualy with improved monitoring of critically ill patients. Nov 2007.
A variety of policies exist to aid the recognition and response of clinical deterioration. National Early Warning Score (NEWS) is a useful and widely used tool through-out the UK. Developed to facilitate early detection of deterioration by giving a numerical score (0 to 3) for each vital sign. Royal College of Physicians,2012). The total score is defined as the early warning score. This allows nurses to escalate and obtain medical opinion on specific trigger points but also to use a common language and a standardized assessment of the patent’s severity illness.
The Royal College of physicians (2017), when creating the NEWS gave a particular attention to sepsis saying that :”the NEWS could be used to better identify patients likely to have sepsis who were at immediate risk of serious clinical deterioration and required urgent clinical intervention”. Although in intensive care this tool is not used, as we monitor our patients very closely and our monitors tell us any changes constantly, it is always helpful as guide in critical care.
Sepsis can be defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection”. In particular we talk about septic shock when blood pressure drops to a dangerously low level after an infection. For a burn patient this condition is common and the main reason is that our patients have lost their primary barrier, the skin, which protects the body from environmental pathogens. For this reason, the infection can persist and their body is continuously exposed to inflammatory mediators as long as the wound remains open. In addition these patients develop a profound hypermetabolic response that can persist for months and which leads to having persistent tachycardia, tachypnea, leukocytosis, and reset their normal temperature to around 38 °C. In other words, a baseline burn patient will always have typical characteristics of a common septic patient.
A definition of sepsis for burns patients can be defined in the table below;
Table 1; American Burn Association (2007)
• Temperature (>39°C or <36°C),
• Progressive tachycardia (>110 beats per minute),
• Progressive tachypnea (>25 breaths per minute not ventilated or minute ventilation >12 L/minute ventilated),
• Thrombocytopenia (<100,000/μl; not applied until 3 days after initial resuscitation),
• Hyperglycemia (untreated plasma glucose >200 mg/dl, >7 units of insulin/hr intravenous drip, or >25% increase in insulin requirements over 24 hours),
• Feed intolerance >24 hours (abdominal distension, residuals two times the feeding rate, or diarrhea >2500 ml/day).
During the description of this incident, I will use the Airway, Breathing, Circulation, Disability and Exposure assessment.
This is considered the best approach applicable to all clinical areas in all emergencies. This tool is helpful to ensure that critical illness is promptly recognized and appropriated managed. Resuscitation Council (UK) (2015)
Names involved in the scenario have been changed to maintain anonymity and patient confidentiality in according with the Code of Conduct for Nurses and Midwifes ( 2015).
Case study:
Sophie was a 23-year-old female admitted in Burns intensive care with 55 % full thickness burn to her legs, lower back and arms, due to an accident in Qatar. Day 65 with us, no past medical history or co morbidities. The patient came to us with an infection in her wounds already diagnosed in Qatar caused by a multi-resistent bacteria except for one antibiotic.
Airway and management
Sophie had a surgical tracheostomy in situ, size 7. The tracheostomy was inserted for different reasons: wean from the ventilator as part of the dead space that is present in the endotracheal tube is avoided, weaning from sedation, be able to speak , and more suitable for oral hygiene and oral nutrition.
During the airway assessment I first checked if the tracheostomy was well secured and in place inserting one finger between her neck and the tie. I noticed that the tie was wet after the shower so I changed it with the help of the doctor to avoid any complication, making sure this was not too tight and appropriately secured. It is important that both medical and nursing staff are present during this procedure so they can be able to reinsert the tracheostomy in case of accidental decannulation. (Tracheostomy management, May 2014).
Cuff pressure was checked with a cuff manometer to make sure was between 20-30 cmH2O, the cuff read 24 cm H2O. A good measurement of the cuff pressure is imperative in order to prevent any damage to the tracheal mucosa but also to avoid any air leakage from the ventilator. (March 2007- Best practice statement)
Sophie’ s inner tube was clean and patent, free from blockage and secretion. In non-ventilated patients the inner cannula should be regularly removed, cleaned or changed at a maximum interval of 4 hourly in a patient with a productive chest, and at least 8 hourly in all cases (TRACHEOSTOMY CARE INTENSIVE CARE SOCIETY STANDARDS 2014).
A Tracheostomy will bypass the natural humidification of the upper airway, for this reason it is necessary to maintain a well humidified and heated airway. This principle applies to both room air and assisted ventilation. The Swedish nose device heats and moistens the gases. The Swedish nose was replaced after the shower to ensure this was dry and clean. I was happy with Sophie’s airway that was secure and patent.
Breathing and management
On assessment, Sophie’s oxygen saturation was 92%, on two L/min of oxygen, the patient appeared drowsy, eyes opened in response to voice commands although unable to respond verbally. According to The British Thoracic Society a normal oxygen saturation needs to be > 94%, in particular for critically ill patients high concentration of oxygen should be administered immediately to achieve a target saturation of 94-98%.(2017).
Monica and Melbye(2015) observed that lower values from pulse oximetry were associated with increased mortality in the general adult population.
Her respiratory rate (RR) was 27, therofore higher than the normal range of 12-20 breaths per minute.
She had equal chest expansion although demonstrated increased work of breathing with use of accessory muscles. She appeared non cyanotic. On auscultation she had bilateral airway entry with no added sounds. Placing both hands to her chest I noticed she didn’t have any abnormalities but a symmetrical chest expansion . I obtained an arterial blood gas as the patient was desaturating fast and no breathing properly.
An arterial blood gas result can help in the assessment of a patient’s gas exchange, ventilatory control and acid–base balance.
Arterial blood gas results: Normal Values
PH-7.27 PH-7.35-7.45
PaO2-8.5 10.6-13.3 kPa
PCO2-3.9 4.6-6 kPa
BE- -12 -2-+2
HCO3- -18 22-28mmol/L
Lactate-4. 0-2mmol/L
The arterial blood gas was suggestive of metabolic acidosis with partial respiratory compensation.
7The partial arterial pressure of oxygen was lower then the normal range as the saturation of oxygen. The partial pressure of oxygen, also known as PaO2, is a measurement of oxygen in the arterial blood. It shows how well oxygen is able to move from the lungs to the blood.
Oxygen saturation varies with the PaO2 in a nonlinear relationship and is affected by temperature, pH, 2,3 diphosphoglycerate, and PaCO2. According with Arun Madan (May-June 2017) the oxy–hemoglobin (Hb) dissociation curve reflects the cooperative interaction between Hb and oxygen (O2) molecules. The most important aspect of the curve is that as the oximeter reading falls below 90%, the PaO2 drops very rapidly and the O2 delivery to the tissues is also reduced. This can be correlated with irreversible brain damage and cardiac arrest.
In pathological conditions such as sepsis, tissue oxygenation is compromised and associated with decreased Po2.ref
The patient was trying to blow off her CO2 increasing her RR.The respiratory centre in the brain responds to changing levels of carbonic acid in the blood. When the acid level of blood increases and is not controlled by the first buffer system, the respiratory system responds.
Hyperventilation causes the body to exhale and “get rid of” CO2 from the blood, through the lungs. This is how the body responds to excess acid in the blood.(ref)
The renal system is another powerful buffer system. As the blood pH decreases (more acidic), the kidneys will compensate by retaining HCO3.(jan 2016).
Our assessment found it necessary to start the mechanical ventilation on bi pap mode with high flow oxygen. As the patient was too weak breath unassisted. BIPAP mode can provide pressure conrolled ventilation which allows unrestrictive spontanious breathing. ref
According with Hormann C.,Benzer. H,with the BIPAP mode (Biphasic Positive Airway Pressure), the patient can breathe freely even under the most invasive ventilation conditions.
It can provide pressure-controlled ventilation in a system which always permits unrestricted spontaneous breathing, but It can also be viewed as a Continuous Positive Airway Pressure (CPAP) system with a time-cycled change of the applied CPAP level.
Sophie was sedated to aid comfort and compliance of mechanical ventilation using Propofol.
Before starting the sedation I explained to Sophie about our plan and that she would be sedated and no longer able to communicate, although she was to sick to pay attention or talk. I also tried to reassure her holding her hand and saying that everything would be fine.
Communication in intensive care is always a challenge in particular when the patient is too unwell and sedated. All nurses and the members of stuff should improve their skills learning about techniques and technology available for intubated patients.
We started also to monitor her End Tidal CO2 via capnography to make sure she was well ventilated (Capnography is most often used to ensure correct placement of the endotracheal tube (The intensive care foundation 2015))and to understand better her compensatory mechanism.
I soon informed the nurse in charge and another anesthetist giving a brief description of what was happening. I used the SBAR communication tool (situation, background,assessment, recomandation) which is a structured communication system that enables information to be transferred accurately between individuals, it is very useful in an emergency scenario because the communication is focused on what is really important without losing time.
Circulation and management
• While the doctor was finishing to set up all the settings and the alarms on the ventilator, I started my circulation assessment but I soon noticed that Sophie blood pressure (measured by the arterial line) was very low ( BP: 80systolic/49 diastolic mmhg with a Map of 50 mmhg). A systolic blood pressure <90 mmhg and a dyastolic BP <50 mmhg is considered hypotension which means vital organs are not well perfused. MAP or mean arterial pressure, is defined as the average pressure in a patient’s arteries during one cardiac cycle. It is a good indicator of perfusion to vital organs than systolic blood pressure (SBP). True MAP can only be determined by invasive monitoring and complex calculations; however it can also be calculated using a formula (MAP = [ (2 x diastolic) + systolic ] divided by 3). There are several clinical situations in which it is very important to monitor the mean arterial pressure. In patients with sepsis, vasopressors are often titrated based on the MAP. The guidelines of the Surviving Sepsis Campaign, recommend A MAP ≥ 65 mmHg in patients with severe sepsis and septic shock. A MAP ≥ 60 mmHg is believed to be needed to maintain adequate tissue perfusion.
Systemic hypotension in sepsis is related to different factors. According to Takakura et al nitric oxide, produced by the edothelium during hypoxia can cause vascular hyporeactivity to vasoconstrictor agents and myocardial dysfunction. During sepsis vasodilation and inflammation occurs, the pathogenic microorganism stimulates the release of cytokines and fluid leaks from the circulation into the interstitial tissue, for this reason there is a decrease of intravascular volume that lead to hypotension and inadequate tissue perfusion.
I checked the position of the trasducer, that needs to be in line with the right atrium and I have recalibrated it. The arterial line was patent and the bag of normal saline connected to the trasducer was full and in date.
The three leads ecg were already well attached to the patient chest during and after the shower, Sophie was tachycardic, her heart rate was 130 beat per minute on sinus rhythm. As described by the American Heart Association, a normal heart rate should be between 60-100 bpm. This increasing of HR can be viewed as a compensatory mechanism due to her low blood pressure. Every change in blood pressure is detected by the baroreceptors located in the aortic arch that stimulate the sympathetic nervous system by increasing the heart rate.
Her lactates (from the previous ABG) were 4. Elevated lactate indicates anaerobic respiration. There is a relationship between elevated blood lactate and tissue hypoxia, as explained by Jan Bakker and Pinto de Lima in those patients with clinical shock, associated with tachycardia, hypotension, cold and clammy skin and decreased urine output, lactate levels have been referred to as the best objective indicator of the severity of shock. The use of lactate as a clinical prognostic tool was first suggested in 1964 by Broder and Weil when they observed that a lactate excess of > 4 mmol/L was associated with poor outcomes in patients with undifferentiated shock (oct 2013)
Accordin with Jen Bakker (2003) lactate is a normal end product of glycolysis (Fig. 1). It can only be formed from pyruvate mediated by lactate dehydrogenase [1].
Lactate can only be metabolized by the conversion to pyruvate. Therefore, blood lactate levels depend on pyruvate metabolism. Both oxidation of pyruvate and gluconeogenesis require the presence of oxygen. Consequently when oxygen levels fall, glucose is mainly converted to lactate.
I had also a quick look to Sophie’ s core temperature through the monitor while I was concentrated on her blood pressure. Her core temperature was 41 celsius degrees. According to Victor E. Del Bene. a normal body temperature is considered to be 37 C degrees and pyrexial if the oral temperature exceeds 37.5 C degrees or the rectal temperature exceeds 38 C degrees.
As mentioned before, patients with severe burns are considered apyretic also with a temperature of 38 celsius degrees.
In the same time I asked to my colleague to check her capillary refill time (CRT) (pressing a finger’s tip for 5 seconds and than releasing it), while I was still paying attention to Sophie’s blood pressure. Her CRT was 4 seconds.
CRT is a good indicator of peripheral perfusion. A normal CRT is between 1 to 2 seconds, above 2 seconds we talk about poor perfusion due to peripheral vasoconstriction as a consequence of low blood pressure and hypoperfusion.(2015)
I measured quick Sophie’s urine output via her urine catheter, her urine output was 0 mls/kg/hr from one hour and 0.3 mls/kg/hr from the previous hour. In normal conditions a normal urine output ihas to be 0.5 mls/kg/hr, if lower then 0.5 mls7kg7hr for two hours or more, this can compromise quick the renal function and for this reason needs to be immediately escalated to the doctor.
Urine output is a marker of acute kidney injury (AKI) and a good guide for fluid resuscitation. Matthieu Legrand and Didier Payen explain that a decrease of urine output may be associated to a decrease of glomerular filtration rate due to decrease of renal blood flow or renal perfusion pressure. As mentioned before, Sophie’s MAP was very low and considering also her low urine output Sophie was at risk of AKI.
As suggested by the surviving sepsis campaign (2015) I started immediately with fluid resuscitation giving 250 mls of Hartman solution IV (crystalloid solution) with a rate of 1200ml/hr, followed by another bolus of Hartman at the same rate. Sophie’s blood pressure was still the same so we carried on with another bolus of Hartaman followed by one bolus of albumin. Albumin (colloid) was given as the patient was requiring a substantial amount of crystalloids with no changes, according to G. Clemente et al. thanks to its electrostatics properties, albumin reduces the endothelial permeability and remains in the bloodstream longer. Its efficacy is still now matter of debate. In patients with severe sepsis, treated with albumin and crystalloids compared with ones treated with crystalloids only, an increase in survival was not observed.(2015)
After giving a total of 750 mls of crystalloids and other 250 mls of colloids the patient was still not responding to fluids, so at that point we decided to administer noradrenaline (vasopressor) infusion in order to maintain the mean arterial pressure of 65 mmhg and above.The surviving sepsis campaign recommend noradrenaline as first choice for the management of septic shock.
Following the Surviving Sepsis Care Bundles (2015) , we applied vasopressors (noradrenaline) after giving fluids and we started to give her three different kind of intravenous antibiotics defined as “rescue” antibiotics as per microbiology plan, suggested in case of sudden deterioration. The use of multiple antibiotics with the specific intent of covering the know or suspected pathogen(s) with more than one antibiotic is indicated in order to accelerate the pathogen clearence rather than to broaden antimicrobial coverage(Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2016)
According with the Surviving Sepsis Care Bundles and another sub-bundle called “Sepsis Six”, blood culture were obtained by the doctor from a peripheral stab and from the Central Venous Catheter because her temperature was higher then 39.5 as per unit protocol.
The Surviving Sepsis Campaign Bundles created these “bundles” to simplify the complex processes of the care of patients with severe sepsis. A bundle is a group set of elements of care that, when implemented together, have an effect on outcomes beyond implementing the individual elements alone.
Surviving Sepsis Care Bundles 2015
TO BE COMPLETED WITHIN 3 HOURS OF TIME OF PRESENTATION:
Measure lactate level
Obtain blood cultures prior to administration of antibiotics
Administer broad spectrum antibiotics
Administer 30ml/kg crystalloid for hypotension or lactate ≥4mmol/L
TO BE COMPLETED WITHIN 6 HOURS OF TIME OF PRESENTATION:
Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65mmH. In the event of persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion and document findings according to Table 1.
Re-measure lactate if initial lactate elevated.
The sepsis six is a bundle that deal with basic therapies that has been shown to improve outcomes in septic patients if followed within the first hour after recognition of sepsis.
SEPSIS SIX
Administer high-flow oxygen to maintain target oxygen saturations greater than 94% (or 88%-92% in people at risk of hypercapnic respiratory failure)
Take blood cultures
Give intravenous antibiotics
Start intravenous fluid resuscitation
Check lactate level
Monitor hourly urine output.
My patient has been constantly monitored during and after all these interventions and re-assessed.
Her blood pressure was now 102/50 mmHg with a MAP of 68 mmHg
HR-110 bpm
Her temperature was now 39 Celsius degrees
CRT 2 seconds
O2 Saturation 98 %
RR was 20 ( patient on bipap)
Lactates 2.4 mmolls
Blood sugar level 6.5mmols
At this point we carried on with noradrenaline adjusting the dose depending on her Map, we applied some ice on all her body to decrease her body temperature and we also gave some paracetamol. I also asked the doctor to review all her medications in particular those that could make the blood pressure low.
Sophie’s blood sugar was within the normal range. Burned patient may experience hyperglycemia caused buy increased metabolism and inflammation. This condition as Gabriel A. Mecott et Al have described has been associated with an increased risk of morbidity and mortality in critical ill patients.
In general critically-ill patients with hyperglycemia have a higher incidence of infections and sepsis especially wound infections, pneumonia and bacteremia.(2010)
Disability
After stabilizing my patient’s cardiovascular conditions, I assessed her neurological status using the Glasgow Coma Scale (GCS). This standardized tool is used to assess the patient’s level of consciousness and is essential for the recognition of the cognitive impairment due to brain damage.