[Previous article][Contents][Next article]
| Priscilla Reid is a fifth year Registered Nurse in the Intensive Care Unit, St. Vincent's Hospital, Sydney. |
This Case Study focuses upon a single, 33 year old male of Anglo-Saxon extraction. Mr. Boyd was admitted to the Intensive Care Unit (ITU) following an amyl nitrite overdose, with methaemoglobinaemia. Emphasis is placed upon his medical and nursing care whilst he was in ITU.
[top]
To set the scene, it is necessary to recap on the events preceding his admission to the ITU. On the third of June 1992, an ambulance was summoned to premises in Surry Hills on behalf of Mr. Nicholas Boyd (pseudonym). Mr. Boyd was found on the floor of a steam bath, unconscious, blue and in a pool of vomit. Immediate treatment included insertion of an oropharyngeal airway, ventilation via the Black Bag and administration of one litre of hartmans via a peripheral cannula. Intravenous (IV) naloxone 2mg and nebulised ventolin were also administered.
Shortly after arrival in the Accident and Emergency Centre (AEC), Mr. Boyd had a bradycardic arrest, he was intubated, Cardiac Pulmonary Resuscitation (CPR) was commenced and IV adrenaline administered with successful rapid return of cardiac output. In view of a bottle of amyl nitrite being found next to Mr. Boyd's body and his chocolate brown skin colour, a provisional diagnosis of amyl nitrite overdose was made, with subsequent methaemoglobinaemia. Upon stabilisation, methylene blue was given and Nicholas was transferred to ITU.
[top]
Volatile nitrites are popular recreational drugs (Romeril & Concannon, 1981). They are available over the counter at Eastern Sydney chemists and can be purchased at most sex shops in Kings Cross. Users claim the drug gives them an immediate high. They express feelings of disinhibition, high excitement, power and a rush of sexual stimulation (Medical Journal of Australia, 1981). Nitrites dilate blood vessels throughout the body by a direct relaxant effect on smooth muscle. Amyl nitrite is used medically to dilate the coronary vessels and to reduce blood pressure. Amyl nitrite along with other nitrites has the capacity to convert haemoglobin to methaemoglobin. Methaemoglobin is formed by oxidation of the Ferrous (Fe2+) iron of haemoglobin to the Ferric (Fe3+). That is from a state where haemoglobin can pick up oxygen to a state where it cannot and therefore impairs unloading of oxygen to the tissues (Franklin-Bunn, 1991).
We are all exposed to nitrites and the average individual has a methaemoglobin level of one per cent to one-point-five per cent. Cyanosis occurs when 15 per cent of haemoglobin has been converted to methaemoglobin, but symptoms of headache, dizziness, weakness and dyspnoea are not likely to occur until the concentration reaches 30-40 per cent. At levels of 60 per cent stupor and respiratory depression occur and the blood is chocolate coloured. A level greater than 60 per cent represents a life threatening situation (Dreishach and Robertson, 1987). Mr Boyd's methaemoglobin level was initially 94 per cent!
[top]The treatments available for methaemoglobin are administration of methylene blue, exchange transfusion and hyperbaric oxygen (Haddock & Winchester, 1983). Mr. Boyd received eight millilitres of one per cent methylene blue in and a further 10 millilitres in ITU. Methylene blue is rapidly converted to a leuko base by the coenzyme diphosphopryridine nucleotide (DPN). This leuko base rapidly reduces Ferric Iron (Fe3+) to Ferrous Iron (Fe2+).
|
+ DPN |
|
+ Leukomethylene Blue |
Mr. Boyd's colour improved rapidly following the methylene blue and exchange transfusion was unnecessary. Exchange transfusions simply replace methaemoglobin with haemoglobin. A third alternative is hyperbaric oxygen which has been shown to reduce methaemoglobin levels and mortality in mice (Haddad & Winchester, 1983). This treatment was not considered for Mr. Boyd.
[top]
On admission to ITU at midnight, Mr. Boyd's clinical picture was as follows (normal range):
Clinical Pathology
[top]
Clinical Observations
The patient was intubated with an oral endotracheal tube (ET) whilst in AEC. The chest X-ray revealed the end of the ET tube to be correctly positioned at 2 cm above the carina and mid aortic-knuckle. It was noted how many centimetres this was at the lips and written in the care plan. The tube was tied according to protocol, ensuring a secure airway and minimal ulceration to the lips. A hi-lo tube was chosen to reduce tracheal necrosis, and decrease the risk of aspiration by the conforming nature of the cuff. The reservoir was three quarters inflated and was not impinging on the outer plastic covering, no leak was heard. The oral ET tube was suctioned to ensure patency. Aspirated gastric contents were suctioned. The fact that gastric contents were aspirated reinforces the importance of a good seal.
[top]
The size 9 oral endotracheal tube was attached to the Erica ventilator with the following parameters:
Hourly observations ensured an 800ml tidal volume, controlled airway pressures and the correct number of mechanical breaths. Listening with a stethoscope, air entry was noted to be equal. Hourly checks of the humidifier ensured the patient was receiving humidified and warmed oxygen. Chest X-ray revealed right lower lobe opacities consistent with probable aspiration. Hourly suctioning with size 14 straight and angled catheters ensured patency of the tube and removed secretions. By applying a PEEP of 7.5 cm H20, positive pressures opened up the fluid filled alveoli to maximise gaseous exchange.
In the absence of oxygen, anaerobic metabolism prevailed resulting in a build up of lactic acid. Mr. Boyd was hyperventilated with an IMV of 14 and FiO2 of 100% due to his severely hypoxic state. Sodium bicarbonate 8.4% IV 50 mmol x 2 was administered as a buffer to soak up excess acid in his tissue and blood. Coincidentally, a low PCO2 was desired to activate a respiratory compensation for his severely metabolic acidotic state.
Blood gases were taken hourly and ventilator settings were changed according to arterial blood gas results. The FiO2 was weaned by increments of 10 per cent over six hours to 40 per cent. The IMV 14/minute and PEEP 7.5 cm H20 remained unchanged over night. Due to his initial hypothermia and severely hypoxic state, pulse oximetry was not possible and a reading would have been misleading. The pulse oximeter is not an efficient measurement of oxygen saturation of arterial blood in the context of methaemoglobinaemia as it does not have the sophistication to discern the altered haemoglobin state. It can only recognise haemoglobin with oxygen attached and without oxygen attached. Therefore it is possible for the oximeter to read a high saturation reading when there is almost no oxyhaemoglobin present. PaO2 is a more reliable diagnostic measurement when high levels of methaemoglobin are present (Gaivin, 1992). By 3.00am Mr. Boyd's methaemoglobin level was 18 per cent and his oxygen uptake was adequate to allow oxygen saturation measurement (Sa02). A level greater than 90 per cent was always maintained.
[top]
Originally hypotensive in AEC, Mr. Boyd's haemodynamic status responded quickly with colloids and aramine 3 mg. In ITU, adequate MAP was maintained without further colloids or drugs - in fact he had trends of hypertension. Intravenous therapy by a peripheral cannula was continued for hydration and drugs. Blood pressure, mean arterial pressure, temperature, heart rate and colour were continuously monitored. MAP between 70 to 110 Hg was accepted to ensure adequate tissue profusion. Hourly urine output of at least half to one millilitre per kilogram per hour was maintained to ensure adequate level of hydration and desired perfusion of the kidneys. A rectal temperature probe was inserted to measure his core temperature. Mr Boyd's temperature climbed from 32.5°C to 36°C over four hours. This was achieved by the heating of humidified air and placing a space blanket over warm blankets to reduce conductive and convective heat loss.
Long term hypothermia is detrimental as it increases the body's oxygen requirements, results in sluggish perfusion of the brain and causes arrhythmias. Arrhythmias were a further concern considering the possibility of Mr. Boyd ingesting unknown arrhythmic causing drugs. A 12-lead electrocardiogram (ECG) reflected no abnormalities and demonstrated normal sinus rhythm. Mr. Boyd was continuously monitored on the ECG monitor for arrhythmias and the effect of hypoxia on the myocardium.
Skin colour was particularly dramatic in the case. Upon presentation in AEC the attending Resident Medical Officer described Mr. Boyd's colour as chocolate brown. Mr Boyd pinked up quickly following the methylene blue administration and colour returned to normal over five hours. Return to normal colour and normal capillary filling reflects the binding of oxygen to haemoglobin and the delivery of oxygen to the tissues with desired perfusion. Thromboembolic deterrent stockings were fitted to aid venous return and prevent deep vein thrombosis.
A secondary examination in AEC eliminated rhabdomyolysis, a common consequence of drug overdose, when the patient lies in one position for an extended period. Whilst in ITU, Mr. Boyd was repositioned every second hour from side to side, to protect his skin, to eliminate potential pressure sores and to ventilate both lungs.
[top]
Hourly neurological observations reflected a rapid improvement following the Methylene blue administration in conjunction with hyperventilation. The consequence of hypoxic brain damage was eliminated when Mr. Boyd scored 11-12 on the Glasgow coma scale within four hours of arriving in ITU.
General Nursing Care of the Unconscious Patient
Despite a depressed level of consciousness, consideration of Mr. Boyd's emotional well being was a high nursing priority. Mr. Boyd was constantly reassured and explanations given before any invasive procedure. Tone was non-judgmental and privacy was respected. General nursing care included second hourly mouth and eye care. Mr. Boyd had chronic diarrhoea and required regular washes. Due to Mr Boyd's unknown reaction with increased levels of consciousness, bed rails were always up when the area was unattended and he was physically restrained with Chinese fingers for his own protection. A nasal swab was taken to screen MRSA. The indwelling catheter, nasogastric tube and the rectal probe were well anchored and cannula site was observed for redness and swelling. The nasogastric tube was aspirated fourth hourly. The stomach was protected by the administration of sixth hourly sucrolfate. Prophylactic vitamins were also administered.
[top]
Mr. Boyd's recovery was dramatic. Within seven hours of his arrival in ITU, his clinical picture was as follows:
Clinical Pathology
Clinical Observations
Mr. Boyd was extubated and oxygen therapy was applied via the Puritan mask at 6 litres per minute. Post extubation "look, listen and feel" observations were applied. Mr. Boyd had equal air entry, respiratory rate was 18 beats per minute and expired air was evident. The flow rate was reduced, arterial blood gases were excellent and Mr. Boyd no longer required supplementary oxygen therapy, or intensive care management. Mr. Boyd was seen by the physiotherapist and encouraged to do deep breathing and coughing exercises.
[top]
Mr. Boyd's form of identification was an employment card with his picture and name. Mr. Boyd was seen by the social worker who deemed it unnecessary to pursue a next of kin in the context of Mr. Boyd's excellent prognosis. The social worker maintained that ringing up Mr Boyd's place of employment would jeopardise his relations with his employers. A friend visited Mr Boyd on the 4th June and her contact number was written in the care plan. Pastoral services were offered to Mr. Boyd, but he declined. The drug and alcohol team were referred to Mr Boyd to discuss his drug dependence and the seriousness of his previous night's actions. Mr. Boyd was very embarrassed by the overdose and claimed it was atypical behaviour.
[top]
The most significant side effect of an amyl nitrite overdose is the development of methaemoglobinaemia. In Mr. Boyd's situation, it was life threatening. The medical and nursing principles immediately applied are routine for any unconscious patient. Care and control of airway, breathing and circulation. Then specific to any drug overdose is the administration of the specific anti-dote, which in this case was methylene blue. The normal principle of reducing the absorption or increasing the excretion of a toxin was not applicable because the nitrite was inhaled. Mr. Boyd had decreased levels of consciousness and required complete physical and psychosocial protection. These areas were suitably recognised and appropriate care and emotional support was provided. The outcome of the medical and nursing care that Mr. Boyd received in ITU was a complete recovery with no neurological or emotional deficits. He was discharged from ITU on 5 June, 30 hours following his admission.
[top]
[top]