Survival from Drowning

Treatment at the scene of an accident is sometimes of little ultimate consequence with many disorders, but in drowning it often determines whether the victim lives or dies. The standard of first aid and resuscitation training of the rescuers therefore influences outcome.

In human drowning, deterioration after initial resuscitation is frequently recorded, and this influences management (see Chapter 23).

The temperature of the water and thus the degree of hypothermia may also be factors. Poorer results are achieved in warm water drowning.

In what was previously referred to as ‘dry’ drowning (in which the distal airway remains relatively dry because of early laryngospasm), the patient is hypoxic and, if rescued in time, may– make a rapid recovery. However, when laryngospasm relaxes and fluid aspiration occurs as it eventually does if the victim remains immersed, the result is drowning.

Other factors that influence outcome include the following: the presence of chlorine, other chemicals and foreign bodies; the aspiration of stomach contents; and the subsequent development of pneumonitis, respiratory infection and multi-organ failure.

One likely cause for delayed death is progressive lung injury2. ARDS develops in a significant proportion of drowning cases; usually hours or days after the aspiration. Other causes of death in the days after the event include cerebral hypoxia, secondary infections (usually of the lungs), renal failure and iatrogenic events.

Factors that negatively influence survival have been well documented by Modell:

  • Prolonged immersion.
  • Delay in effective cardiopulmonary resuscitation.
  • Severe metabolic acidosis (pH <7.1).
  • Asystole on admission to hospital.
  • Fixed dilated pupils.
  • Low Glasgow Coma Scale score (<5).

Nevertheless, none of these predictors is infallible, and survival with normal cerebral function has been reported with all the foregoing factors.

Claims of survival after extended duration underwater without ventilation of the lungs have been used to encourage rescuers to persevere with resuscitation efforts. There have been cases reported in victims who have been submerged for between 15 and 45 minutes4–7 and who have survived without neurological sequelae. The explanations given for such prolonged durations of survival are as follows:

1. Hypothermia is protective and develops very rapidly with aspiration of water. In swimmers and divers, hypothermia may be present before the incident.

2. The ‘diving reflex’ is a possible, but contentious, explanation. Within seconds of submersion, the diving reflex may be triggered by sensory stimulation of the trigeminal nerve and by reflex or voluntary inhibition of the respiratory centre in the medulla. This produces bradycardia and shunting of the blood to the areas more sensitive to hypoxia – the brain and coronary circulations. It is independent of baroreceptor or chemoreceptor inputs. The diving reflex is more intense in the frightened or startled animal, compared with animals which dive or submerge voluntarily, but it is not known whether this finding is applicable to humans. Water temperatures higher than 20°C do not inhibit the diving reflex, but progressively lower temperatures augment it.

3. Gas exchange in the lungs can continue after submersion. With or without the effects of laryngospasm, there may be several litres of air remaining within the lungs, thus allowing for continued exchange of respiratory gases. Increased pressure (depth) transiently enhances oxygen uptake by increasing the PO2 in compressed lungs. In an unconscious state, with low oxygen use and the effects of hypothermia, a retained respiratory gas volume could add considerably to the survival time, although it is not often considered in the literature on drowning.

Whether fluid enters the lungs in an unconscious victim depends on many factors, including the spatial orientation of the body. For example, a dependent position of the nose and mouth, facing downward, is not conducive to fluid replacement of the air in the lungs.

Even though spectacular and successful rescue can be achieved after prolonged submersion, it is more frequent that this is not so. Many victims lose consciousness and die after only a few minutes of submersion.

Clinical Features of Drowning

The respiratory manifestations of drowning include the following:

  • Dyspnoea.
  • Retrosternal chest pain.
  • Blood-stained, frothy sputum.
  • Tachypnoea.
  • Cyanosis.
  • Pulmonary crepitations and rhonchi.
  • Hypoxaemia.

Pulse oximetry typically reveals low oxygen saturations, but a pulse oximeter may not read at all on a cold, peripherally shut-down victim. An arterial blood gas determination reveals hypoxaemia (lower limit of the ‘normal’ range for arterial oxygen tension [PO2] is 80 mm Hg [10.5 kPa]). There is often acidaemia that usually has a metabolic component, but that may be mixed and very severe in a respiratory peri-arrest situation. Carbon dioxide levels are frequently elevated in a peri-arrest condition, but they may be normal or even low during spontaneous breathing or manual ventilation.

Initial chest x-ray studies may be normal, or they may show patchy opacities or pulmonary oedema. Significant hypoxia may be present even when chest x-ray changes are subtle or even absent.

Complications may include pneumonitis, pulmonary oedema, bronchopneumonia, pulmonary abscess and empyema. Severe pulmonary infections with unusual organisms leading to long-term morbidity have been reported. Progression to the acute respiratory distress syndrome (ARDS) is not uncommon in drowning situations.

Central nervous system effects of hypoxia include variable impairment of consciousness, ranging from awake to comatose, with decorticate or decerebrate responses. If hypoxia is prolonged, a global hypoxic brain injury can result with cerebral oedema, raised intracranial pressure and sustained coma. Seizure activity is common in this setting.

Cardiovascular manifestations are largely the result of the effects of hypoxaemia on the heart. Progressive bradycardia leading to asystolic cardiac arrest is not uncommon. After rescue and resuscitation, supraventricular tachycardias are frequent, but various other dysrhythmias may occur. When the hypoxic acidotic insult has been severe, hypotension and shock may persist despite re-establishment of a perfusing rhythm. The central venous pressure may be elevated as a result of right-sided heart failure exacerbated by elevated pulmonary vascular resistance, rather than by volume overload. Mixed venous oxygen tension may also be low, indicating tissue hypoperfusion.

Multi-system organ failure may develop secondary to the hypoxaemia, acidosis and resultant hypoperfusion. Decreased urinary output occurs initially and occasionally progresses to acute tubular necrosis and renal failure. Haemoglobinaemia, coagulation disorders and even disseminated intravascular coagulation may complicate the clinical picture.

Laboratory findings include decreased arterial oxygen with variable PaCO2 values, metabolic and respiratory acidosis, haemoconcentration, leucocytosis, increased lactic dehydrogenase, occasional elevated creatinine levels and haemolysis as indicated by elevated free haemoglobin. Serum electrolytes are usually within the normal range.

The arterial oxygen tension is always low, but the carbon dioxide tension may be low, normal or elevated.

Recovery from drowning is often complete in survivors. However, residual neurological deficiencies may persist in the form of either cognitive impairment or extrapyramidal disorders.

Pathophysiological of Drowning

The effects of drowning are multiple, but the initial and primary insult is to the respiratory system, with hypoxaemia being the inevitable result (Case Report 22.1).
The sequence of events that occur with drowning includes the following:

Initial submersion in water preventing air breathing. This is usually followed by voluntary breath-holding. Duration of the breath-holding depends on several factors, which include general physical condition, exercise, prior hyperventilation and psychological factors (see Chapter 61). This is frequently a period when the victim swallows substantial amounts of water.

Fluid aspiration into the airway at the point of breaking the breath-hold. Eventually, the rising arterial carbon dioxide tension (PaCO2) compels inspiration, and fluid is aspirated. Laryngeal spasm may follow the first contact of the glottis with water. While laryngospasm is maintained, the lungs may remain dry; however, the inevitable result of the associated hypoxaemia is that the spasm will eventually also break, and if the victim remains immersed, then aspiration of water into the lungs will follow. Vomiting of swallowed liquid may occur, and this may also be aspirated into the lungs.

Progressive hypoxaemia. This may initially result from oxygen use during voluntary breath-holding and any subsequent laryngospasm, but ultimately it is aspiration of water or regurgitated stomach contents into the gas-exchanging segments of the lungs that provokes persistent and progressive hypoxaemia. The inhalation of water can occur through involuntary diaphragmatic contractions even if the victim is not breathing per se. The presence of water instead of air and the dilution of surfactant function with consequent alveolar atelectasis result in a ventilation-perfusion (V/Q) mismatch with a preponderance of low V/Q units and extensive venous admixture. The resulting hypoxaemia leads to unconsciousness, bradycardia and ultimately asystolic cardiac arrest. Hypoxic brain damage follows within a very short space of time.


CASE REPORT 22.1

Ernie Hazard, age 35: ‘I was thinking “This is it. Just take a mouthful of water and it’s over.” It was very matter of fact. I was at a fork in the road and there was work to do – swim or die. It didn’t scare me. I didn’t think about my family or anything. It was more businesslike. People think you always have to go for life, but you don’t. You can quit….’

The instinct to breathe underwater is so strong that it overcomes the agony of running out of air. No matter how desperate the drowning person is, he or she does not inhale until on the verge of losing consciousness. That is called the ‘break point’.
The process is filled with desperation and awkwardness: ‘So this is drowning…so this is how my life finally ends…. I can’t die, I have tickets for next week’s game’…. The drowning person may even feel embarrassed, as if he or she has squandered a great fortune. He or she has an image of people shaking their heads over this dying so senselessly. The drowning may feel as if it is the last, greatest act of stupidity in his or her life. The thought shrieks through the mind during a minute or so that it takes the panicky person to run out of air.

Occasionally, someone makes it back from this dark world. In 1892, a Scottish doctor, James Lowson, was on a steamship bound for Colombo. Most of the 180 people on board sank with the ship, but Lowson managed to fight his way out of the hold and over the side:

‘I struck out to reach the surface, only to go further down. Exertion was a serious waste of breath and after 10 or 15 seconds the effort of inspiration could no longer be restrained. It seems as if I was in a vice which was gradually being screwed up tight until it felt as if the sternum of the spinal column must break. Many years ago my old teacher used to describe how painless and easy death by drowning was – “like falling about a green field in early summer” – and this flashed across my brain at the time. The “gulping” efforts became less frequent and the pressure seemed unbearable, but gradually the pain seemed to ease up. I appeared to be in a pleasant dream, although I had enough willpower to think of friends at home and the site of the Grampians, familiar to me as a boy, that was brought into my view. Before losing consciousness the chest pain had completely disappeared and the sensation was actually pleasant.

‘When consciousness returned I found myself on the surface. I managed to get a dozen good inspirations. Land was 400 yards distant and I used a veil of silk and then a long wooden plank to assist me to shore. On landing and getting on a sheltered rock, no effort was required to produce copious emesis. After the excitement, sound sleep set in and this lasted three hours, when a profuse diarrhoea came on, evidently brought on by the sea water ingested. Until morning break, all my muscles were in a constant tremor which could not be controlled’.

From Junger S. The Perfect Storm. London: Fourth Estate; 1997, with quotes from James Lowson in The Edinburgh Medical Journal.